Una D. McCann
Anxiety is the term applied to a psychophysiologic state characterized by worry (apprehensive expectation), muscle tension, autonomic hyperactivity, and hypervigilance. Anxiety may improve performance in response to danger or challenge and, thus, may serve an adaptive function. However, when excessive or inappropriate in form or context, it leads to subjective distress and impairment in social and occupational functioning. Anxiety can be caused by a number of medical illnesses (e.g., hyperthyroidism, pheochromocytoma), and the presence of anxiety can prolong or exacerbate medical conditions (e.g., irritable bowel syndrome [IBS]). There is also some evidence that anxiety, like depression, may be an independent risk factor for the development of certain conditions, such as cardiovascular disease, hypertension, irritable bowel syndrome, and migraine headaches (1,2).
Normal Illness-Related Anxiety
Patients visiting their health care providers or awaiting the results of tests are often anxious. Although such anxiety may be understandable and realistically related to concerns about the meaning of symptoms and consequences of disease, it nonetheless requires recognition and management because it may interfere with medical care. For example, it has been found that survivors of myocardial infarction (MI) and their spouses recollect little of the information given to them during in-hospital convalescence, partly as a result of anxiety (3). Such findings highlight the importance of detecting normal illness-related anxiety and treating it skillfully. The following approaches are helpful:
Drug-Related Anxiety
When evaluating patients with symptoms of anxiety, it is important to identify all medications or substances taken during or just before the onset of symptoms of anxiety. Prescribed drugs, over-the-counter (OTC) preparations, caffeine, ephedra-containing cold medications or dietary supplements, “herbal” preparations, alcohol, and other substances can all cause symptoms similar to those found in the primary anxiety disorders described later in this chapter. Licit and illicit stimulants, such as methylphenidate, amphetamine, cocaine, and 3,4-methylenedioxymetham phetamine (MDMA or “ecstasy”) can produce symptoms indistinguishable from those of idiopathic anxiety disorders.Table 22.1 lists common examples of such compounds.
When considering the role of caffeine in producing anxiety, it is helpful to know the approximate amount of caffeine in commonly consumed beverages and substances:
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TABLE 22.1 Drugs and Other Substances That May Exacerbate (or Produce) Anxiety |
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Patients who experience prominent anxiety, panic attacks, obsessions, or compulsions in relation to the ingestion of these substances are classified by the American Psychiatric Association as having a substance-induced anxiety disorder. However, because individuals with an anxiety disorder, particularly panic disorder, are more susceptible to the anxiogenic effects of stimulants (4), the clinician should be vigilant for an underlying idiopathic pre-existing anxiety disorder in patients with substance-induced anxiety.
Anxiety Disorders
The anxiety disorders are a group of psychiatric conditions in which anxiety is the predominant symptom. Anxiety causes distress and dysfunction because it is excessive, unrealistic, or inappropriate in form or context. The five major anxiety disorders are panic disorder, obsessive-compulsive disorder (OCD), phobia (specific, social, or agoraphobia), posttraumatic stress disorder (PTSD), and generalized anxiety disorder (GAD). As a group, the anxiety disorders are the most common psychiatric illnesses in the United States, affecting an estimated 19 million American adults (5). In addition to existing in their “pure” forms, individual anxiety disorders are frequently comorbid with other psychiatric conditions, including other anxiety disorders, affective disorders (Chapter 24), somatoform disorders (Chapter 21), substance use disorders (Chapters 28 and 29), and eating disorders (Chapter 11). Although adjustment disorder with anxiety is not classified as an anxiety disorder, this condition is frequently encountered by primary physicians and should be considered in the differential diagnosis of anxiety. Therefore, a brief description of adjustment disorder with anxiety is provided here before the anxiety disorders are reviewed.
Adjustment Disorder with Anxiety
Description
The term adjustment disorder with anxiety is used when excessive and maladaptive anxiety occurs in response to a recent, identifiable stressor. This “reactive” anxiety resolves when the stressor remits or when the patient reaches a new level of adaptation or adjustment.Chapter 24, Table 24.1 lists American Psychiatric Association criteria.
Case Study
A 55-year-old married man presented to the office because of non-exertional chest pain, dizziness, and breathlessness. He had suffered a heart attack 3 months before but had recovered uneventfully. A recent stress test had shown no signs of coronary insufficiency or serious arrhythmia. His wife reported that the patient had not been himself since leaving the hospital and that “every little thing gets on his nerves.” Although he had formerly been “on the go all of the time,” he was now afraid to go out of the house. Physical examination now showed no evidence of heart failure, and the electrocardiogram (ECG) was unchanged. The physician reviewed the encouraging results of the ECG and treadmill test, reassured the patient about his symptoms, explained that anxiety is common after MI, and asked the patient to enroll in a cardiac rehabilitation program, to telephone in 1 week to report on his symptoms, and to return to the office in 2 weeks for followup examination and a review of his progress. The physician also demonstrated some simple relaxation techniques (seeNonpharmacologic Approaches, Self-Regulation Techniques) and gave the patient a small supply of lorazepam to be used on an as-needed basis.
Epidemiology, Origins, and Natural History
Estimates of the point prevalence of adjustment disorder are highly variable, ranging from 5% to 20%, dependent upon the population evaluated. Adjustment disorder is believed to be equally common in males and females. By definition, an adjustment disorder with anxious mood must begin within 3 months of a precipitating stressor and last no longer than 6 months after the stressor (or its consequences) ceases.
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Treatment
Management includes the following steps:
Panic Disorder
Description
The hallmark feature of panic disorder is the occurrence of panic attacks—discrete episodes of extreme anxiety—accompanied by a variety of physical and emotional symptoms. To meet the criteria for a panic attack, the episode must comprise at least four symptoms in addition to intense fear or discomfort. Symptoms of panic include palpitations, sweating, trembling, shortness of breath, feeling of choking, chest pain or discomfort, nausea or abdominal distress, dizziness, derealization (feelings of unreality) or depersonalization (feeling detached from oneself), paresthesias, chills or hot flushes, fear of losing control or going crazy, and fear of dying. In addition to the involvement of panicky feeling and physical/emotional symptoms, panic attacks must reach peak intensity within 10 minutes after their onset.
The presence of repeated, unexpected panic attacks is necessary but not sufficient for the diagnosis of panic disorder. As described later, a number of other anxiety disorders as well as mood disorders are sometimes associated with panic attacks. In contrast to other disorders, panic disorder requires that, after the experience of a panic attack (or attacks), the affected individual is persistently (for at least 1 month) worried about having another panic attack or concerned about the significance or consequences of the panic attack.
Patients with panic disorder have significantly increased utilization of both outpatient and inpatient general medical services. Utilization of primary care services by patients with panic disorder is approximately three times higher than that of the average patient and is higher than that of patients with other psychiatric illnesses, such as major depression (2,6). The prevalence of panic disorder may be increased in several medical conditions, including labile hypertension (7), mitral valve prolapse (8), asthma (9,10), chronic obstructive pulmonary disease (COPD) (11), and migraine headache (12,13).
Approximately one third of individuals with panic disorder develop agoraphobia, or fear and avoidance of places and situations where a panic attack might occur or escape would be difficult (14). If the agoraphobia is left untreated, the number and extent of avoided situations can expand and generalize, rendering the patient housebound. Agoraphobia can occur in the absence of panic attacks (agoraphobia without history of panic disorder in Diagnostic and Statistical Manual of Mental Disorders, 4th Edition [DSM-IV]); but the latter condition is less commonly encountered in psychiatric clinics than panic disorder with agoraphobia (15). Among patients with panic disorder, those most likely to develop agoraphobia are women who have persistent panic attacks (i.e., no history of clinical remissions), a high degree of interpersonal sensitivity, and a history of anxiety or depression in childhood (15). Table 22.2 summarizes American Psychiatric Assocation diagnostic criteria for panic disorder without and with agoraphobia.
Case Study
A 24-year-old graduate student was referred by the emergency department for recurrent episodes of substernal chest pain, some of which had occurred during sleep. Chest pain was associated with abdominal pain, shortness of breath, and dizziness. Medical workup had revealed no cardiac or endocrine source for the patient's symptoms. The patient reported that during the last semester of graduate school she began experiencing these episodes “out of the blue.” Her first episode took place when she was “pulling an all-nighter studying for her dissertation presentation.” She acknowledged drinking quite a bit of coffee during that period, but since then she had experienced panic attacks while not using caffeine heavily. Although she admitted to some life stressors, such as starting a new job and moving to a new city, she viewed these stressors as positive. The patient reported that since she first began to have panic attacks she had become “obsessed” with the thought that she had some sort of heart condition that would kill her.
The patient stated that she would be agreeable to both medication treatment and “talking therapy.” She was started on a low dose of a selective serotonin reuptake inhibitor (SSRI) and was referred to a cognitive behavioral therapist for short-term (12-week) symptom-focused therapy. Within 6 weeks the patient reported that her anticipatory anxiety had diminished significantly, as had the intensity and frequency of her panic attacks. Within 3 months, she was panic free. She continued taking the SSRI for 18 months, after which it was slowly tapered.
Epidemiology, Origins, and Natural History
The case study illustrates a number of characteristic features of panic disorder. It typically begins in late adolescence or early adulthood, with the median age at onset of 24 years (16). It has a prevalence of 1% to 2% and is twice as common in women as in men (14,16). Many patients with panic disorder experience panic-free remissions,
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particularly after treatment. However, panic disorder is typically a chronic, lifelong condition, and those patients who achieve remission often experience relapses (15). Frequently associated psychiatric conditions include major depression, social phobia, PTSD, GAD, agoraphobia, OCD, and substance abuse (14,17, 18, 19).
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TABLE 22.2 Diagnostic Criteria for Panic Disorder without and with Agoraphobia |
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Patients with panic disorder present special differential diagnostic challenges to generalists and cardiologists. Although panic symptoms are often difficult to distinguish from angina and may lead to unnecessary cardiac catheterization (20), patients with panic disorder have an increased cardiovascular mortality rate (21, 22, 23). Other studies, which were limited by the fact that they included male subjects only, revealed that the risk of sudden cardiac death in patients with panic-like symptoms is as much as six times higher than in patients with low anxiety levels, even when known risk factors for cardiac death (e.g., cholesterol level, tobacco use, family history) are taken into account (2). Additionally, panic symptoms may be simulated by a number of noncardiac medical disorders, including alcohol and sedative-hypnotic drug withdrawal, marijuana use, pheochromocytoma, hyperthyroidism, hypoglycemia, and temporal lobe epilepsy.
Studies support the view that panic disorder is primarily a biologic disorder. Genetic factors have been implicated by family studies demonstrating a tenfold increase in panic disorder among first-degree relatives of panic probands (24) and a higher concordance rate for panic disorder among monozygotic than among dizygotic twins (25). Lactate infusion (26) and hyperventilation (27) may stimulate panic attacks in people with panic disorder, suggesting the existence of specific biologic triggers. Pharmacologic treatments may by themselves dramatically reduce the frequency of panic episodes (see Evaluation and Treatment). Although the neurobiology of panic disorder is not clearly established, preclinical models of conditioned fear, in concert with clinical pharmacologic and neuroimaging studies, have implicated a number of brain regions and neurotransmitters or neuromodulators in the symptoms of anxiety and panic. With regard to brain regions, there are considerable data suggesting that the central nucleus of the amygdala, the orbitofrontal cortex/anterior insula,
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and the anterior cingulate cortex are involved in the expression of fear and anxiety. Among the endogenous neural substances that are believed to be involved in anxiety are norepinephrine, serotonin, corticotrophin-releasing factor, gamma-aminobutyric acid (GABA), and substance P.
There are also learning (or conditioning) theories to explain panic disorder. These propose that panic attacks develop when physical sensations occurring at times of stress are interpreted as signs of grave illness, giving rise to panic. The physical sensations of arousal become conditioned phobic stimuli, provoking the panic symptomatology (conditioned response) (28). Conditioning models have been particularly persuasive in accounting for the development and maintenance of agoraphobia (29).
Evaluation and Treatment
A systematic approach to the evaluation and treatment of panic disorder includes the following steps:
Regardless of the type of antidepressant used for treatment, patients with panic disorder are notoriously sensitive to a variety of medications. It is quite common for a patient with panic disorder, if treated with a “typical” starting dose of an antidepressant (e.g., 50 mg of sertraline or 20 mg of fluoxetine) to develop what is commonly referred to as the “jitteriness syndrome.” Patients report feeling keyed up, or on edge, or as if they had consumed excessive amounts of caffeine. Some patients actually note an increase in the number of panic attacks early in the course of treatment. To avoid severe jitteriness and consequent noncompliance, it is important to educate the patient about this phenomenon in advance and to initiate dosing at lower than typical dosages (i.e., 25 mg sertraline or 10 mg fluoxetine). Doses should not be increased until jitteriness totally resolves. Some patients experience an increase in jitteriness each time the dose is increased, but typically this is a short-lived phenomenon (1 to 2 weeks).
Panic disorder is a chronic, recurring illness. In new-onset panic disorder, it is generally accepted that pharmacotherapy should continue for at least 1 year, at which time medications can be tapered over a 4- to 6-month period for a drug-free trial period (32). It is clear, however, that many patients relapse after medications are discontinued. Patients who have experienced more than one previous relapse should be considered for long-term antidepressant treatment, which has been shown to be effective in preventing relapse (33,34).
Once widely accepted as a first-line therapy for the treatment of panic disorder, benzodiazepines now are generally viewed as a short-term adjunct to therapy by most anxiety disorder experts in this country. Patients who are significantly impaired by their symptoms of anxiety during the period before stabilization on antidepressant are sometimes treated with benzodiazepines as a “bridge” (35). However, this strategy is not always fully successful, because more than 50% of patients have difficulty discontinuing benzodiazepines (36).
Controlled clinical research studies have also demonstrated the efficacy of cognitive behavior therapy (CBT) in the treatment of panic disorder (37). Indeed, CBT has been found, in most studies, to be equally or more efficacious than medication treatment alone, and it can be quite cost-effective. The biggest drawback to CBT, assuming that the patient is willing to make the time commitment to participate, is the paucity of well-trained therapists skilled in administering CBT effectively. As suggested by its name, CBT comprises both cognitive and behavioral therapeutic techniques and is typically administered in 12 sessions over a 12-week period. During this time, patients systematically learn to recognize and correct cognitive distortions associated with their panic attacks (e.g., “When I feel my heart beat quickly, it means that I have a fatal heart problem”) and master relaxation methods to use in the face of mounting anxiety. Because hyperventilation is a
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frequent feature of panic attacks that exacerbates some panic symptoms (and can lead to acroesthesia), most CBT programs for panic involve breathing retraining, wherein patients learn diaphragmatic breathing techniques and how to decrease their respiratory rate when anxious. Finally, CBT often involves interoceptive exposure (i.e., producing physical symptoms, such as dizziness, that are associated with panic and distorted cognitions). If a patient has concomitant agoraphobia, the therapist may also employ exposure therapy techniques, gradually exposing the patient to feared situations as he or she learns to employ cognitive and behavioral methods of panic control.
As with most psychiatric illnesses, an important aspect of the treatment of panic disorder is education of the patient and significant others regarding the nature of this condition. Usually, patients are relieved to learn that panic disorder is a common, treatable disease with a biologic basis. Education by the clinician, supplemented by readily available books written for the lay person, may help reduce the patient's sense of isolation and embarrassment and provide practical advice about managing panic symptoms. The National Institutes of Health (NIH) has an up-to-date website with comprehensive information about all of the anxiety disorders as well as a list of books, web links, and national organizations suitable for professionals and laypersons (see http://www.hopkinsbayview.org/PAMreferences).
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TABLE 22.3 Diagnostic Criteria for Obsessive–Compulsive Disorder |
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Obsessive-Compulsive Disorder
Description
As suggested by its name, the essential features of OCD are obsessions—recurrent, persistent, intrusive thoughts (e.g., “Touching this doorknob will give me a disease”)—and compulsions—purposeful but senseless behaviors or rituals (e.g., washing hands 17 times each morning). The obsessive thoughts are distressing to the patient, who usually is aware that the thoughts are illogical and unreasonable. In an individual patient, obsessions and compulsions are often related, and the compulsive behaviors are conducted in an effort to reduce the anxiety brought on by the obsessive thoughts. However, it is not uncommon for a patient to have a variety of obsessions that have no thematic relationship. It is the presence of obsessions and/or compulsions that distinguishes OCD from obsessive-compulsive personalitydisorder (see Chapter 23), a personality type characterized by meticulousness, perfectionism, and rigidity. Table 22.3 lists the American Psychiatric Association diagnostic criteria for OCD.
Case Study
An 83-year-old widow was referred for evaluation because of disabling fears of contamination. She was a retired mathematics teacher who liked her subject because 1 and 1 always equal 2: “I
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like the certainty.” A practicing Catholic, she recalled that during adolescence she had once delayed disposing of a sanitary napkin because she had sneezed over it after returning home after Mass and worried that bits of the communion wafer might have lodged in it. She had received psychiatric treatment several times for obsessive-compulsive symptoms but had recently been doing well until she was forced to change apartments. After the move she became preoccupied with worries about contamination with germs. Especially vexing was deciding when she had adequately washed her hands after defecating; she was consumed by uncertainty about how long she should wash and how she could safely dispose of the towel after drying her hands. Her main fear was that others might be contaminated and become ill as a result of her carelessness. As a result of these ideas, she washed her hands excessively, did not leave her apartment, ate poorly (so that she would defecate less), and was unable to engage in normal conversation. Treatment consisted of a form of CBT called “response prevention” and the use of an SSRI (see Evaluation and Treatment). Within 2 weeks she showed improvement, and by the end of 8 weeks she was able to dispel obsessive ideas effortlessly and felt no compulsion to wash excessively.
Epidemiology, Origins, and Natural History
One to two percent of people in the community (38) and in the general medical clinic (39) meet criteria for OCD. Its prevalence is slightly higher among women and tends to decline with age. Symptoms usually have their onset in adolescence or early adulthood. In one study of patients with OCD (40), the most common obsessions were fear of contamination (55%), fear of acting aggressively (50%), and fear of performing unacceptable sexual activities (32%). Somatic obsessions were present in 34% of patients, including a woman who performed breast self-examinations 100 times per day to reassure herself that she had not developed breast cancer (40), and 36% had obsessive thoughts involving the need for symmetry. The most common compulsions involved checking, cleaning, and counting. In most cases the symptoms were chronic and continuous, with some tendency for symptomatic worsening during times of stress. Associated psychiatric diagnoses included major depression (30%), simple phobia (7%), and panic disorder (5%).
Explanations for OCD have been advanced from several perspectives. Psychoanalytic writers have viewed obsessive-compulsive symptoms as products of reaction formation against unacceptable wishes and impulses, often related to aggression and sexuality. Behavioral theorists and practitioners have stressed the anxiety-reducing effects of compulsive rituals and have proposed that compulsions are maintained precisely because of their positively reinforcing ameliorating effects on conditioned anxiety. The importance of personality traits in the development of OCD is suggested by data showing that preexisting obsessive traits (e.g., meticulousness, perfectionism, indecisiveness) are very common in clinical samples of patients with OCD (40) and that people who are obsessional, anxious, or self-conscious may be especially vulnerable to the emergence of OCD in response to life change (41).
Other research suggests that OCD has biologic origins. The importance of genetic factors is supported by studies showing high rates of OCD among first-degree relatives of patients with OCD (42) and evidence for a major gene in segregation analyses (43). Clinical studies linking OCD with head trauma (44) and other neurologic disorders (45) add support to the conception that OCD may be a manifestation of brain disease. Of all the anxiety disorders, OCD has been most extensively studied with neuroimaging techniques. Available neuroimaging data, considered together, implicate abnormalities within the cortico-striato-thalamo-cortical network (46). Particularly, patients with OCD tend to have hyperactive orbitofrontal, anterior cingulate, and caudate activity that is further activated during symptom provocation and that is attenuated with treatment (47). It has been proposed that the primary lesion of OCD is located in the corpus striatum (48), an hypothesis that is supported by the finding that autoimmune processes known to damage the striatum can be associated with new-onset OCD (49). Results of functional neuroimaging studies, considered together with genetic, epidemiologic, and pharmacologic data, have led to the hypothesis that prefrontal–basal ganglia–thalamic–prefrontal circuits are particularly important in the pathophysiology of OCD (50). Of great theoretical and practical importance is the demonstration that numerous antidepressants that prevent uptake of serotonin into presynaptic neurons are effective in the treatment of OCD (51). This observation strongly implicates a role for central serotonergic neuronal systems in the pathophysiology of this disorder.
Evaluation and Treatment
A systematic approach to the evaluation and treatment of OCD involves the following steps:
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anxiety. Patients are taught to control their obsessive ruminations by commanding themselves to stop ruminating when obsessive ideas arise (thought stopping), and they are exhorted to resist carrying out their compulsive acts so that they can learn that there are no dire consequences associated with nonexecution of the rituals (response prevention). These techniques are often helpful if patients can be persuaded to practice them.
Generalized Anxiety Disorder
Description
GAD is characterized by persistent and excessive worry that is present more days than not for at least a 6-month period. In addition to excessive, inappropriate, or unrealistic worry, the patient must experience at least three of six physical symptoms, including restlessness, easy fatigability, difficulty concentrating, irritability, muscle tension, and sleep disturbance. Table 22.4 lists American Psychiatric Association criteria.
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TABLE 22.4 Diagnostic Criteria for Generalized Anxiety Disorder |
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Case Study
A 50-year-old woman came to her physician complaining of difficulty swallowing, insomnia, tremor, and loose stools. She reported that she’d been a “worrier” since her 20s, but that this characteristic had increased in the year since her husband died, and she became responsible for managing all aspects of the household. Three of her adult children, one of whom had mental retardation, lived at home, and she continued to prepare their meals and do their laundry. She admitted that she was “scared of everything,” generally tense (“Little things make me jump”), and often experienced feelings of shakiness, diaphoresis, and fluttering in the chest, usually in response to contemplating driving by herself
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or engaging in another feared activity. She did not describe discrete intense panic episodes (see Panic Disorder). She did report feeling blue for the past several months, and that she had difficulty enjoying things. Physical examination, ECG, and exercise stress test results were normal. Although she was reluctant to take medications, she agreed to try treatment with venlafaxine XR, beginning at a dose of 75 mg per day. Additionally, she agreed to meet with her physician on a monthly basis for 12 months for counseling. During counseling sessions she learned simple relaxation techniques (see later discussion), helped construct a program of systematic desensitization regarding driving, and developed a plan to request that her children participate more consistently in the running of the household. At the end of 1 year she was greatly improved. She was driving regularly to visit friends across town with growing confidence.
Epidemiology, Origins, and Natural History
GAD is one of the more common anxiety disorders, with an estimated lifetime prevalence of 5.1% (60). Patients frequently initially present to their general practitioner with a variety of somatic complaints, for which no medical basis is discovered (61). Like all of the anxiety disorders except OCD, GAD is more common in women and usually begins in the early twenties. GAD is a chronic illness that often persists for several decades (61,62). It is relatively uncommon for GAD to exist in isolation; the majority of patients also meet criteria for major depression, another anxiety disorder, or alcohol abuse (63).
The causes of GAD are not fully understood. A number of studies have indicated that there is a mild genetic component to GAD (25,64). A large-scale study in female twins suggested that GAD and major depression share a common genetic basis, possibly explaining the frequent comorbidity of these two illnesses (65). Twin research also suggests that the personality trait neuroticism (a general tendency to experience negative emotions) also shares genetic underpinnings with GAD (66). Traumatic early life experiences, especially the death of a parent (67), may be a predisposing factor, although patients with this disorder do not characterize their childhoods as more difficult than nonanxious people do (68). Events in later life, especially unexpected events perceived as important and negative (69), may also play a role in the emergence of symptoms.
Evaluation and Treatment
A systematic approach to the evaluation and treatment of the patient with GAD includes the following steps:
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Phobias
Description
As a group, phobias are enduring fears of harmless objects or situations (phobic stimuli) that lead patients to avoid contact with them (phobic avoidance). Patients with specific phobia fear discrete objects and situations, such as animals, heights, air travel, needles, and visits to the doctor, whereas patients with social phobia have fears of social humiliation and the scrutiny of others. People with agoraphobiafear being in situations from which escape is difficult or where help may not be available in the event of an anxiety-provoking episode, such as in open or public spaces (literally, fear of the agora or marketplace). Although phobic patients generally recognize their fears to be excessive and unreasonable, they nonetheless seek to avoid the phobic stimulus because exposure provokes intense anxiety. The diagnosis of phobia is made only if avoidance of the feared object or situation leads to social or occupational impairment or if the patient experiences great distress as a result of the symptom.
Tables 22.5 and 22.6, respectively, list American Psychiatric Association criteria for specific phobia and social phobia. Agoraphobia can be seen in a number of anxiety disorders (e.g., social phobia, PTSD) and is described in the section on panic disorder.
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TABLE 22.5 Diagnostic Criteria for Specific Phobia |
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TABLE 22.6 Diagnostic Criteria for Social Phobia |
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Case Study
A 50-year-old married business executive sought treatment because of an addiction to chlordiazepoxide. In his early 20s he had first become aware of his discomfort in large groups, particularly when he was the focus of attention. On occasion, he would experience panic attacks during these large social gatherings. He discovered that regular use of chlordiazepoxide improved his general level of comfort, and by age 50 he was using 80 mg per day routinely. In addition to feeling anxious in large groups, the patient was anxious in small groups when he was the center of attention. He avoided writing checks in public because he was afraid that his hand would tremble or that he would hold up a check-out line. His job required that he occasionally make professional presentations before clients and supervisors. In the days preceding a
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presentation, he would experience substantial anticipatory anxiety associated with the fear that he would be unable to recall what he wanted to say, or that his throat would close up, preventing him from speaking. In response to this fear, he would increase his daily chlordiazepoxide dosage by 50% to 100%. On the day of the presentation he would take 200 to 300 mg and would perform well. He was dissatisfied with this practice because he now felt depressed and believed that the medication might be playing a role. His diagnosis at the time of evaluation was social phobia and benzodiazepine dependence. A slow chlordiazepoxide taper was undertaken and completed within 6 months. At the same time, the patient participated actively in a structured CBT group and was prescribed an SSRI. His social anxiety declined, and his confidence grew as he succeeded in attending parties and giving talks.
Epidemiology, Origins, and Natural History
In recent years, the distinctions among the various types of phobias have received increased scrutiny (77). These include specific phobia(e.g., fear of heights, snakes, blood, insects), circumscribed social phobia (fear of one type of social situation, such as public speaking) andgeneralized social phobia (fear of a number of different social situations). Of the various types of phobia, generalized social phobia is associated with the greatest impairment and is more likely to be present with other psychiatric disorders. Family and twin studies support a genetic contribution in each type of phobia (25).
Specific phobias are characterized by excessive fear of specific objects or situations. When confronted with the feared object or situation, a patient with a specific phobia becomes extremely anxious and may experience a situation-bound panic attack. Most adults with specific phobias recognize that their fear is irrational, but despite this realization, they avoid the object or endure exposure with great difficulty. One survey found that among eight common phobias, the most common fear in women was that of animals, and the most common in men was that of heights (78). Other common phobias relate to enclosed places, blood, snakes, spiders, and various forms of transportation, such as flying in airplanes. Approximately 8% of the adult population suffer from one or more specific phobias during a 1-year period (79). Most adult phobias are chronic, and they generally do not remit without treatment.
Social phobia, also known as social anxiety disorder, is characterized by excessive and persistent anxiety in social situations, including performances and public speaking (80). The basis of the anxiety is that patients are afraid that they will humiliate or embarrass themselves. Often patients are concerned that people will notice certain embarrassing physical symptoms, such as perspiration, blushing, trembling, or tremulous voice. When placed in unavoidable social situations, patients with social phobia can have panic attacks. In contrast to panic disorder, the panic attacks in social phobia are not “out of the blue.” Further, although patients with panic disorder are concerned about the symptoms of the panic attack (e.g., believe they are having a heart attack), patients with social phobia are concerned that others will notice that they are having a panic attack. Like both panic disorder and specific phobias, social phobia is often characterized by significant anticipatory anxiety. Social phobics can suffer for days or weeks before the feared social interaction.
The lifetime prevalence of social phobia is approximately 13.3% (60). This number includes both patients with circumscribed and those with generalized social phobia. Like most anxiety disorders, social phobia is more common in women than in men and typically begins in childhood or adolescence. It is frequently comorbid with other psychiatric illnesses, including the affective disorders (41.4%), other anxiety disorders (56.9%), and substance abuse disorders (39.6%) (79). As with panic disorder, patients with social phobia have an increased risk of certain medical conditions (e.g., peptic ulcers) and make more frequent use of medical resources than others in the general population (81). Generalized social phobia is a chronic, often lifelong condition (81).
Patients with social phobia may become addicted to alcohol or to sedative-hypnotics as a result of self-directed efforts to ameliorate their social anxiety. Furthermore, phobias and phobic anxiety may be risk factors for ischemic heart disease and other forms of cardiovascular morbidity. There is a significant association between measures of phobic anxiety (fears of enclosed spaces, illness, going out alone, heights, and crowds) and the probability of subsequent ischemic cardiac events (82). Such relationships may be mediated by anxiety-related hyperventilation, which has been shown to cause coronary vasospasm and cardiac ischemia (83), or by anxiety-induced arrhythmia (84).
Treatment
Approaches to treatment of specific phobia are based on the notion that phobic avoidance is maintained by the anxiety-preventing consequences of the avoidance. The treatment of phobias has advanced greatly with the development of behavioral therapies aimed at extinguishing phobic anxiety and phobic avoidance. Three commonly used techniques are desensitization, participant modeling, and social skills training.
Systematic desensitization begins with the gradual exposure of the patient to increasingly vivid and anxiety-provoking mental images of the phobic stimulus. As anxiety is generated, the patient induces relaxation by use of a relaxation technique (see Non-pharmacologic Approaches, Self-Regulation Techniques). By exercising a response incompatible with anxiety (i.e., relaxation) in reaction to the phobic stimulus, the patient gradually extinguishes the phobic anxiety. This treatment occurs
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over a series of sessions until the patient is comfortable enough to encounter the stimulus in vivo. Related to systematic desensitization isflooding or implosion, in which the imagery is presented suddenly rather than gradually.
In vivo desensitization involves gradual, stepwise exposure of the patient to the feared stimulus in real life. The patient is often initially accompanied by the therapist or a trained family member. Progress from less to more anxiety-producing tasks is accomplished by mastering anxiety at each level. The basis for the technique is that repeated exposure leads to extinction of phobic anxiety.
Participant modeling is a form of in vivo desensitization in which the therapist models the desired interaction with the feared object. This kind of procedure may be useful with patients who have a severe needle phobia and whose avoidance of needles may be potentially life-threatening (e.g., in patients requiring insulin). Therapy involves the following steps (85):
Behavioral techniques such as these have been used successfully to treat phobias related to hemodialysis and needles. They may be carried out by nonphysicians and are usually effective within 15 sessions or less. Among patients treated by these techniques, phobias, hypochondriacal symptoms, and work adjustment often improve within 6 months, and visits to health care providers decrease markedly (86,87).
Social skills training is not always an appropriate treatment for phobias, including social phobia. Cognitive behavioral treatment of social phobia often involves exposure to social situations. The issue is not necessarily lack of social competence; rather, it is getting over unrealistic anxiety regarding humiliation and embarrassment.
Specific phobias are typically treated with the CBT methods described previously. Some patients with prominent sympathomimetic symptoms (e.g., tremor, diaphoresis, palpitations) in isolated performance situations benefit from treatment with β-adrenergic blockers, administered the day of the performance situation. These individuals should always initially take low doses (e.g., 25 to 50 mg of atenolol) and should have a test dose days or weeks before use in the performance situation. This “practice” dose serves to reassure the patient that he or she will not experience untoward effects and that the dose is not excessive (e.g., associated with disabling drops in blood pressure). Social phobia can be effectively treated by either use of CBT (individual or group) or medications. CBT for social phobia involves correcting distorted cognitions (e.g., “The audience will see me perspire and blush and will think I am incompetent”) and teaching behavioral techniques (e.g., progressive muscle relaxation) to use in the face of social anxiety. As with most forms of CBT, treatment for social phobia is time limited (typically 12 weeks) and focuses on the symptoms of social phobia rather than interpersonal conflicts or long-standing psychological issues.
At present, the first-line medication treatment for generalized social phobia is an SSRI, although monoamine oxidase inhibitors (MAOIs), high-potency benzodiazepines, and the anticonvulsant gabapentin have also been demonstrated to be efficacious (88, 89, 90). Some of the newer-generation antidepressants also show significant promise for the treatment of generalized social phobia, although they have a less well-established track record than the SSRIs do (91).
Posttraumatic Stress Disorder
Description
People who have been exposed to a traumatic event that involved potential death or serious injury to themselves or another sometimes develop a syndrome characterized by intrusive recollections or dreams of the event, avoidance of stimuli provoking memories of the event, and a heightened level of arousal. Such symptoms are relatively common immediately after a severe trauma. However, if the symptoms persist at least 1 month at a fairly severe level, a diagnosis of PTSD is appropriate. Table 22.7 summarizes American Psychiatric Association criteria.
Case Study
A 45-year-old mechanic sustained burns on the arms and thorax when an engine exploded during repair. He had no history of psychiatric disorder. His surgical treatment was successful, leaving him with little residual physical disability. However, after discharge he experienced marked sleep disturbance, generalized anxiety, and loss of interest in usual activities. He avoided proximity to fire in any form and could not tolerate listening to reports about fires on the radio. Treatment with an SSRI aided sleep, improved his mood, and reduced the frequency of his intrusive memories and recurrent dreams, but it did not affect his avoidance behavior. On the anniversary of his injury he would not leave his room because he could not be persuaded that it was safe to do so.
Epidemiology, Origins, and Natural History
About 3.6% of U.S. adults ages 18 to 54 years (5.2 million people) have PTSD during the course of a given year (NIMH,http://www.hopkinsbayview.org/PAMreferences). In men, the full syndrome is usually found among war veterans who were injured in combat; in women, the most
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common precipitant is physical assault. Individual posttraumatic stress symptoms (particularly nightmares, feelings of jitteriness, and sleep disturbances) are much more common, occurring in approximately 15% of the population. Combat, physical assault, seeing someone being hurt or die, and experiencing a serious threat or close call are the most common traumatic experiences associated with such symptoms (92). The highest rates of poststress disorder are found among women who are victims of violent crime, especially rape (93). For reasons that are not entirely clear, PTSD is more common in women than men (94,95).
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TABLE 22.7 Diagnostic Criteria for Posttraumatic Stress Disorder |
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People with PTSD are twice as likely as people without PTSD to have another psychiatric disorder, particularly OCD, dysthymia, substance abuse, bipolar affective disorder, or antisocial personality. There is also an increased risk of PTSD among people with a history of childhood behavioral problems, especially lying, stealing, truancy, vandalism, and school expulsion. Among people with a history of four such behaviors, 6% met formal criteria for PTSD and 29% reported at least one symptom (92).
National Comorbidity Survey respondents who met criteria for PTSD had 40% elevated odds of high school and college failure, 30% elevated odds of teenage child-bearing, 60% elevated odds of marital instability, and 150% elevated odds of unemployment at the time of the survey, compared with people without PTSD (95,96). Some of these correlates could reasonably be expected to be a result of PTSD.
Explanations of PTSD have been advanced from several perspectives. From the behavioral viewpoint, the posttraumatic symptoms (e.g., hyperarousal, intrusive recollections) are viewed as products of classically conditioned linkages between innocuous stimuli (e.g., a news report about a fire) and the original traumatic event (e.g., painful
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injury in a fire). The avoidance symptoms are explained in terms of operant conditioning: Avoidance of stimuli reminiscent of the traumatic event is reinforced by resulting protection of the patient from the symptoms of phobic anxiety (i.e., hyperarousal). Biologic theorists have proposed explanations involving changes in central adrenergic autonomic arousal (97) and in cerebral mechanisms regulating sleep cycles (98). Neuroimaging studies implicate right cerebral limbic and paralimbic areas in the symptoms of PTSD, with hyperreactivity of the amygdala in response to reminders of the trauma (47). Potential roles for personality traits and early life experiences have been suggested by observations of burn patients and other trauma victims demonstrating relationships between maladaptive personality traits, early life loss, trauma, behavioral problems, and poor posttraumatic adjustment (92,99).
Treatment
Behavioral, psychotherapeutic, and pharmacologic treatment approaches have all been advocated for the treatment of PTSD. Behavioral treatments such as desensitization are generally required to help patients overcome the conditioned avoidance of stimuli reminiscent of the traumatic event. Psychotherapy is virtually always needed to assist patients in dealing with anger about the injury, guilt about survival, and similar themes common among people with PTSD. There is some evidence that early cognitive-behavior therapy diminishes subsequent PTSD symptoms, if not the disorder (100,101).
Antidepressant and anxiolytic medications have been used with variable efficacy. Tricyclic antidepressants and monoamine oxidase inhibitors may be effective in ameliorating hyperarousal, intrusion, and avoidance symptoms and in relieving concurrent major depression (102,103). Several studies have demonstrated the utility of SSRIs for the treatment of PTSD (104). Benzodiazepines are sometimes used, but there is no empiric evidence for their effectiveness in this setting, and they are relatively contraindicated in patients who are at high risk for chemical dependency. Neuroleptic drugs are almost never indicated.
Treatment of Anxiety Disorders: General Measures
Specific treatments have been described for each specific anxiety disorder. This section describes nonpharmacologic and pharmacologic measures that may be of use in several of the anxiety disorders.
Nonpharmacologic Approaches
A variety of cognitive and behavioral interventions are useful in the treatment of anxiety disorders, some of which are listed here.
Education and Explanation
Patients with panic attacks, obsessions and compulsions, posttraumatic distress symptoms, social anxiety, and generalized anxiety often feel different, isolated from others, and confused about the nature of their malady. They benefit greatly from learning that they have a diagnosable disorder, that they are not alone in their suffering, and that there are effective treatments. Patients should be encouraged to contact the NIMH (see http://www.hopkinsbayview.org/PAMreferences) for free and up-to-date science-based information on the anxiety disorders.
Self-Regulation Techniques
Many patients benefit from learning specific techniques that reduce motor tension, hyperarousal, and autonomic hyperactivity. These self-regulation techniques include muscle relaxation, diaphragmatic breathing, biofeedback, self-hypnosis, and meditation exercises (105). Interested generalists can develop skills in teaching these techniques to their patients. Alternatively, patients can be referred to behavioral therapists for instruction.
In progressive muscle relaxation and diaphragmatic breathing (Table 22.8), patients learn to ameliorate anxiety by sequential contraction and relaxation of muscle groups or by slow inhalation using the diaphragm. With regular practice, patients can apply these techniques in times of distress and achieve considerable relief. Commercially available audiotapes are available to help guide patients through the procedure (see http://www.hopkinsbayview.org/PAMreferences); the book, The Relaxation Response (106), is written for the layperson and may also be useful.
In biofeedback training (107), patients learn to control anxiety with the aid of electromyographic information provided to them in the form of visual or auditory messages. During treatment sessions, electrodes are placed in a muscle (e.g., frontalis) or muscle group. Patients then attempt to reduce muscle tension, receive immediate feedback about the effectiveness of their efforts (e.g., reduction in amplitude of a tone fed back to them through earphones), and learn to alter their technique to achieve more complete electromyographic (and clinical) relaxation.
Self-hypnosis training often begins with office-based sessions during which the therapist uses a standard hypnotic induction technique and then, for example, asks the patient to notice a warm, tingling feeling starting in the legs and feet and spreading slowly throughout the body. Pleasant, peaceful mental images might be suggested. Patients are taught to induce these states on their own and are advised to practice them regularly, reinforced by periodic office visits for reassessment and further practice. Clinicians may develop skills in performing hypnosis by attending seminars such as those sponsored by the Society for Clinical and Experimental Hypnosis.
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TABLE 22.8 Essential Steps in Progressive Muscle Relaxation, Rapid Muscle Relaxation Techniques, and Diaphragmatic Breathing Exercises |
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Meditation techniques, such as Zen, yoga, or transcendental meditation, have been practiced for centuries. They have recently become popular treatments for anxiety because they favorably alter anxiety-related physiologic variables such as respiratory rate, oxygen consumption, and galvanic skin response, a measure of autonomic activity. Meditation techniques that are effective in ameliorating anxiety include or encourage the following elements (108):
Pharmacologic Treatments
Individual pharmacologic treatments for the various anxiety disorders have already been discussed. Generally, the SSRIs are a reasonable first-line treatment choice for all of the anxiety disorders, with the possible exception of GAD, for which buspirone may be an acceptable first choice. However, data demonstrating the efficacy of venlafaxine in the treatment of GAD suggest that it may be an excellent first-line choice as well (71,72). Also, given that GAD is commonly comorbid with depression and other anxiety disorders, the combination of buspirone with an SSRI or other antidepressant may be indicated.
Guidelines for use of SSRIs and antidepressants are described elsewhere in this text (see Chapter 24). As noted earlier, when treating new-onset panic disorder or GAD, clinicians often prescribe benzodiazepines as a bridge to help relieve anxiety in patients during the period of titration of antidepressant therapy. Typically, high-potency benzodiazepines such as lorazepam or clonazepam are used for this purpose. Generally, the initial dosages should be low (e.g., 0.25 mg lorazepam every 8 hours or 0.25 mg clonazepam twice daily). Patients should be warned not to drink alcohol or engage in activities such as driving when first using benzodiazepines. Some patients develop a
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central nervous system (CNS) toxicity even at low dosages of these drugs, and patients should be vigilant for this adverse effect. Although pharmaceutical manufacturers and the U.S. Food and Drug Administration (FDA) recommend that benzodiazepines be used only on a short-term basis (i.e., days to weeks) (109), approximately 90% of benzodiazepines sold in the United States in 1990 were used by people reporting daily use for 4 months or longer (110). This may be related to reports indicating that long-term benzodiazepine users have difficulty discontinuing medication and use benzodiazepines to avoid withdrawal (111). Because of the risk of tolerance and dependence, clinicians should limit the duration of benzodiazepine use to the minimal period required for adequate relief of acute anxiety symptoms.Table 22.9 displays usual dosages and pharmacokinetic properties of the various benzodiazepines.
In recent years, the popularity of herbal remedies and “natural” dietary supplements has grown significantly (see Chapter 5). A number of these dietary supplements are purported to relieve symptoms of anxiety, including kava-kava, valerian root, and St. John's wort. Although none of these alternative treatments has yet been proved effective by FDA standards, there is growing acceptance that they may be useful for the treatment of anxiety disorders, particularly in less severe cases. Patients often do not view these substances as “medications” and may not report their use to their primary caregiver. Therefore, the primary care physician should inquire about use of herbal dietary supplements, particularly before initiating treatment with pharmaceutical-grade medications. “Natural” herbal supplements can be psychoactive and are often metabolized by pathways similar to those of pharmaceutical medications. Drug interactions (occasionally severe) and additive effects have been reported in patients who simultaneously used prescription drugs and herbal or non-herbal supplements (seeChapter 5, Table 5.4). Therefore, caution should be exercised in prescribing drugs to patients who are taking supplements. Patients taking kava-kava who are prescribed anxiolytics and patients taking St. John's wort who are prescribed SSRIs should be advised to taper their herbal supplement before initiating treatment with the prescribed medication.
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TABLE 22.9 Usual Dosage and Pharmacokinetics of Anxiolytic Benzodiazepines |
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During the next few years, several new agents may become available for the treatment of anxiety disorders. Among these are corticotropin-releasing factor antagonists and substance P antagonists, both of which have shown promise in preclinical models of anxiety. Several pharmaceutical companies are developing these agents for potential use in anxiety disorders and depression.
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Specific References*
For annotated General References and resources related to this chapter, visit http://www.hopkinsbayview.org/PAMreferences.
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