CHAPTER 32 Anxiety Disorders: Panic, Social Anxiety, and Generalized Anxiety

Charles T. Taylor, MA, Mark H. Pollack, MD, Richard T. LeBeau, BA, Naomi M. Simon, MD, MSc

• Anxiety disorders are the most prevalent mental health problem in the United States, and are associated with marked distress and functional impairments in multiple domains.

• Anxiety disorders commonly co-exist with other psychiatric and medical conditions, which often bodes poorly for the course and prognosis of the disorder.

• Routine screening for anxiety disorders in medical settings is essential; people with anxiety disorders frequently seek treatment at primary care and mental health clinics, and anxiety symptoms often mimic common medical conditions.

• The pathogenesis of anxiety disorders likely resides in the interaction of innate biological vulnerabilities and specific environmental events or stressors.

• Advances in our understanding of the neurobiological and psychological processes involved in the etiology and persistence of anxiety disorders have contributed to the development of effective pharmacological and psychological interventions for many anxiety disorders.

• Despite current efficacious interventions, many individuals with anxiety disorders fail to respond to first-line treatments or do not achieve high end-state function, highlighting the need for continued efforts directed at elucidating the pathophysiological processes relevant to anxiety.

OVERVIEW

Anxiety disorders are the most common mental health problem in the United States, affecting 18.1% of adults in the general population in a given year,¹ and 28.8% of adults at some point during their lifetime.² Recent estimates suggest that anxiety disorders cost the United States more than $42 billion per year, which amounts to almost one-third of the total direct and indirect mental health “bill” for the United States.³ Anxiety itself is a universal human experience; moreover, it is often a normal and beneficial reaction to stressful situations. Determining when anxiety becomes pathological, that is, when it deviates from a normal or expected emotional response to an environmental event, can be informed by considering the following criteria: (1) excessiveness (i.e., “Would the degree of anxiety experienced be considered disproportionate in relation to the person’s current life circumstances or to identifiable environmental stimuli?”); (2) intensity (i.e., “How marked is the level of distress experienced by the person?”); (3) duration or chronicity (i.e., “Does the anxiety response persist for longer than would be expected under the circumstances?”); and (4) impairment (i.e., “To what degree is there evidence of significant impairments in social, occupational, educational, health, or daily function?”). For the diagnosis of an anxiety disorder to be made, the presence of a specific symptom profile associated with a significant level of distress or impairment is required.

Anxiety is manifest in physical, affective, cognitive, and behavioral domains. Physical expressions of anxiety typically reflect autonomic arousal and include characteristic symptoms (such as palpitations, shortness of breath, muscle tension, dizziness, upset stomach, chest tightness, sweating, and trembling). Emotional manifestations of anxiety range from feelings of uneasiness and edginess to terror and panic. Cognitive manifestations of anxiety include worry, apprehension, and thoughts regarding emotional, bodily, or social threat. Behaviorally, anxiety triggers a multitude of responses concerned with diminishing or preventing the perceived threat and associated distress; these include avoidance, escape, and safety-seeking behaviors. The American Psychiatric Association’s (APA’s) Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) separates the anxiety disorders into discrete categories based on purported similarities in phenomenology, etiology, and pathophysiology. Here, we review three common anxiety disorders: (1) panic disorder (PD), (2) social anxiety disorder (SAD) (or social phobia), and (3) generalized anxiety disorder (GAD). Other anxiety disorders are discussed elsewhere in this volume (obsessive-compulsive disorder [OCD], Chapter 33; posttraumatic stress disorder [PTSD], Chapter 34). Common pharmacological and psychological treatments for anxiety-related conditions are reviewed in Chapter 41.

PANIC DISORDER

Although officially introduced into the diagnostic nomenclature in 1980 with the publication of the DSM-III, investigations into the phenomenology and treatment of panic-like symptoms appeared decades earlier. Descriptions of panic disorder (PD) have remained relatively stable across different versions of the DSM, with the cardinal feature of this condition being the presence of recurrent, unexpected panic attacks accompanied by cognitive sequelae (e.g., anxious apprehension) and behavioral sequelae (e.g., interoceptive and situational avoidance) related to perceived consequences of the panic. PD is recognized as a common and often chronic psychiatric condition associated with negative outcomes in emotional and physical health, as well as significant disruptions in several areas of a person’s life. Of all the anxiety-related conditions, PD has been most intensively studied over the past several decades, with considerable advancements being made in our understanding of the psychopathology, neurobiology, and treatment of this condition.

Clinical Characteristics and Diagnosis

The characteristic feature of PD is the presence of recurrent panic attacks, or paroxysms of extreme anxiety, which are sudden, intense bursts of anxiety or fear accompanied by an array of physical symptoms (e.g., rapid heart rate, dizziness, shortness of breath, sweating, and nausea; see Table 32-1 for a complete list of associated symptoms). Panic attacks themselves are relatively common in the general population, with lifetime prevalence rates reported at approximately 28% in a recent large-scale community sample.⁴ The diagnosis of PD, however, requires the presence of recurrent panic attacks (at least some of which have been unexpected), along with at least 1 month of persistent worry about the possibility of future attacks, worry about the implications or consequences of panic attacks, development of situational avoidance, or other behavioral changes that occur due to the attacks (e.g., repeated emergency department [ED] or physician visits due to fears of an undiagnosed medical condition) (see Table 32-2 for the DSM-IV diagnostic criteria of PD). Further, the person must experience marked levels of distress or functional impairment (or both) that result from his or her panic symptoms. The difference between people who experience transitory panic episodes and those who go on to develop the full-blown disorder may be explained by differences in preexisting biological, psychological, or environmental vulnerabilities (see the pathophysiology section later in this chapter). Figure 32-1 illustrates a feedback cycle common in PD.

Table 32-1 DSM-IV Criteria for Panic Attacks

A discrete period of intense fear or discomfort, in which four (or more) of the following symptoms develop abruptly and reach a peak within 10 minutes:

• Palpitations, pounding heart, or accelerated heart rate

• Sweating

• Trembling or shaking

• Sensations of shortness of breath or smothering

• Feeling of choking

• Chest pain or discomfort

• Nausea or abdominal distress

• Feeling dizzy, unsteady, light-headed, or faint

• Derealization (feelings of unreality) or depersonalization (being detached from oneself)

• Fear of losing control or “going crazy”

• Fear of dying

• Paresthesias (numbness or tingling sensations)

• Chills or hot flushes

Table 32-2 DSM-IV Criteria for Panic Disorder

A discrete period of intense fear or discomfort, in which four (or more) of the following symptoms develop abruptly and reach a peak within 10 minutes:

• Presence or absence of agoraphobia

• The panic attacks are not due to the direct physiological effects of a substance (e.g., a drug of abuse or a medication) or a general medical condition (e.g., hyperthyroidism).

• The panic attacks are not better accounted for by another mental disorder.

Figure 32-1 Factors involved in the etiology and persistence of panic disorder.

PD can occur alone or with agoraphobia, which refers to apprehension about having a panic attack in certain situations and avoidance of places or situations where escape or obtaining help in the event of a panic attack would be unlikely or difficult (see Table 32-3 for DSM-IV criteria for agoraphobia). Commonly avoided situations include crowded public places (e.g., malls, grocery stores, or movie theatres), enclosed spaces (e.g., elevators or tunnels), driving, traveling far away from home, and standing in line. The presence of agoraphobic avoidance is believed to represent a more severe form of the disorder and is associated with a variety of poorer outcomes in terms of symptom severity, co-morbidity, and functional impairment.⁴ Hence, most treatment-seeking individuals with PD experience some degree of agoraphobia. Clinically, it is important to distinguish episodes of panic that occur in PD from those that occur exclusively in the context of another Axis I condition. Panic attacks are common in other anxiety-related conditions, and are often characterized by the same physical and cognitive symptom constellation as seen in PD (i.e., they are phenomenologically similar). In the latter cases, however, the source of the fearful sensations is clearly identifiable; that is, the panic attacks are cued or triggered. For instance, panic attacks can be provoked when a socially anxious individual is exposed to situations involving potential observation or evaluation by others, when a person with a specific phobia is exposed to a particular feared stimulus (e.g., heights or spiders), or when a person with PTSD is confronted with reminders of a traumatic event. Conversely, in people with PD, these same types of episodes are experienced, at least initially, as unexpected or as occurring “out of the blue.” Although many patients who seek treatment may describe their panic as being triggered by a particular situation (e.g., being in crowded public places or enclosed spaces, or on public transportation), or activity (e.g., exercising), a thorough history typically reveals the initial onset of panic as occurring unexpectedly, without clearly identifiable triggers. In those cases, the presence of agoraphobia is likely. It is also possible to meet criteria for both PD and another anxiety disorder (with cued panic attacks), as long as there are at least some unexpected panic attacks.

Table 32-3 DSM-IV Criteria for Agoraphobia

• Anxiety about being in places or situations from which escape might be difficult (or embarrassing) or in which help might not be available in the event of having an unexpected or situationally predisposed panic attack or panic-like symptoms. Agoraphobic fears typically involve characteristic clusters of situations (e.g., being outside the home alone; being in a crowd or standing in a line; being on a bridge; and traveling in a bus, train, or automobile).

• The situations are avoided (e.g., travel is restricted) or else are endured with marked distress or with anxiety about having a panic attack or panic-like symptoms, or require the presence of a companion.

• The anxiety or phobic avoidance is not better accounted for by another mental disorder.

Epidemiology

Results from the recent National Comorbidity Survey—Replication (NCS-R) reported lifetime and 12-month prevalence rates of panic disorder at 4.7% and 2.7%, respectively.^2,⁵ Notably, those rates are somewhat higher than findings from the original NCS⁶ and the Epidemiological Catchment Area (ECA) study.⁷ It is unclear whether these discrepancies represent an increasing prevalence over the past several decades, or are due to differences in diagnostic methods and criteria. Given the salient and distressing physical symptoms experienced by people with PD, it is not surprising that prevalence rates of this condition are even higher in primary medical settings, with reports ranging from 3% to 8%.⁸

Despite differences in the reported prevalence of PD over time, the association between PD and several demographic characteristics has remained relatively stable. For instance, PD is consistently diagnosed in about twice as many females as males. PD tends to have an age of onset in late adolescence or early adulthood, although many individuals may exhibit a preexisting history of anxiety-related symptoms in childhood.⁹ Some research suggests a declining prevalence and severity in older adults.¹⁰ For many individuals, the course of the disorder is chronic and unremitting, although symptoms may tend to wax and wane over time.^11,¹²

Impairment and Quality of Life

PD is associated with significant impairments in several spheres of life. Patients with PD report disruptions in work, social, and family function, in addition to having more negative life events and an overall diminished quality of life.¹³ In terms of academic and vocational outcomes, PD is associated with lower educational achievement, a higher likelihood of unemployment, and diminished work productivity. Socially, patients with PD have impaired interpersonal and marital function, and demonstrate increased financial dependency. Moreover, people with PD report greater health-related problems (both physical and emotional),¹⁴ and PD is often associated with excessive health care utilization, often for treatment of nonpsychiatric complaints.^15,¹⁶ It is notable that the degree of impairment and reduced quality of life may be similar to, if not greater than, that of patients with other serious psychiatric (e.g., depression) and medical problems.^13,¹⁷

Co-morbidity

The extant empirical literature suggests that co-morbidity in PD is common, with cases of “pure” PD emerging infrequently in clinical settings. The NCS-R revealed that 83% of the PD-only group and 100% of the PD with agoraphobia group met criteria for one or more lifetime co-morbid conditions.⁴ Co-occurring anxiety disorders were most common (66% for PD only; 94% for PD with agoraphobia), with specific co-morbidity rates as follows: specific phobias (34% and 75%, respectively), SAD (31% and 67%, respectively), PTSD (22% and 40%, respectively), and GAD (21% and 15%, respectively). PD was also commonly associated with the mood disorders, including major depressive disorder (MDD) (35% and 39%, respectively), bipolar disorders (14% and 33%, respectively), and dysthymia (10% and 15%, respectively). Substance use disorders were also common, with alcohol abuse or dependence being diagnosed most commonly (25% and 37%, respectively). Interestingly, impulse-control disorders also frequently occurred with PD, with lifetime co-morbidity rates of 47% and 60%, respectively.

The presence of co-morbidity in PD bodes poorly for a variety of psychological, functional, and treatment outcomes. For instance, increased rates of suicide and suicide attempts have been associated with PD,¹⁴ with some research suggesting that inflated rates of lifetime suicide attempts are the result of co-occurring psychiatric conditions (such as depression or alcohol abuse); however, recent evidence suggests that the presence of PD is associated with increased rates of suicide attempts, even when co-morbidity and a history of childhood abuse are accounted for.¹⁴ Similarly, the lifetime risk of suicide attempts in patients with PD and MDD is more than double that of the two disorders independently.^18,¹⁹ In the case of co-morbid bipolar disorder, anxiety disorders (including panic) have been associated with an earlier age of onset of bipolar disorder, a poorer course of bipolar disorder, a diminished quality of life and function, and heightened levels of suicidal thinking and completion.²⁰ Further, in a sample of patients with bipolar I disorder, the presence of lifetime panic symptoms, in patients with either subsyndromal or full PD, was associated with poor or delayed response to treatment of bipolar disorder.²¹

Given that the symptoms characteristic of PD mimic a variety of medical conditions, it is not surprising that afflicted patients commonly present to EDs or primary care clinics; this is reflected in the high degree of health care utilization associated with this disorder.^16,²² Increased utilization of medical services is even greater in panic-disordered patients with a co-morbid psychiatric condition.²² Furthermore, frequent medical visits are associated to a greater extent with panic-disordered patients compared to those with other debilitating psychiatric conditions, including depression and substance use disorders.²³ It is also notable that panic attacks can occur as a symptom of numerous medical conditions (such as hyperthyroidism and caffeine or stimulant use [e.g., cocaine]). Further, a variety of physical illnesses (such as cardiovascular and respiratory disorders [e.g., mitral valve prolapse and asthma]) often co-occur with but are rarely the direct cause of PD.²⁴

The appropriate detection and diagnosis of PD in medical settings can be complicated given the substantial variability that exists in one’s ability to accurately describe the experience of anxiety. For instance, anxiety-disordered patients may report a diffuse feeling of uneasiness or describe feeling “not right” in their body, and may generate interpretations that something is physically (not psychologically) wrong with them. An additional complicating factor is that many symptoms of panic attacks (e.g., shortness of breath, chest pain, and dizziness) are among the most common complaints of those seeking treatment at medical settings, and research suggests that relatively few patients receive any specific diagnosis for these problems.

Thus, professionals working in a variety of health care settings must be particularly vigilant for potential psychiatric underpinnings of the somatic complaints reported by many patients.

Pathophysiology

Consistent with etiological models of other anxiety-related conditions, the pathogenesis and maintenance of PD are likely the result of a complex interaction of biological, psychological, and environmental factors. In support of a genetic transmission of PD, twin studies have demonstrated that monozygotic twins have a significantly greater concordance rate for PD than do dizygotic twins. Further, the risk of PD is increased eightfold in first-degree relatives of patients with the disorder. A review of twin and family studies suggests that PD has a heritability of approximately 40%, with additional significant contributions from unique environmental effects (greater than 50%), and only a relatively small (less than 10%) contribution from common (familial) environmental factors.²⁵

Stressful life events also appear to be important in the etiology of PD. Some research has found that approximately 80% of patients with PD report major life stressors within the 12 months preceding the onset of the disorder,²⁶ suggesting that stressful life events may contribute to the timing of the onset of the disorder.²⁷ Childhood physical and sexual abuse also appear to increase the risk for the later development of PD.²⁸ Moreover, symptom severity has been correlated with negative life events (including interpersonal conflicts, physical or health-related problems, and work-related difficulties),^29,³⁰ while the presence of chronic life stressors has been shown to worsen the course of panic disorder.³¹ Finally, some work has suggested that teenagers who smoke are at a higher risk of developing PD, although the causal nature of this association remains uncertain.³² All in all, the extant literature supports a diathesis-stress model of PD, suggesting that exposure to life stressors may trigger a preexisting vulnerability toward panic.

Neurobiology

Interest in the underlying neurobiology of PD has grown since the longstanding observation that infusion of sodium lactate provoked panic attacks in patients with PD but not in controls. Since then, a large body of research has demonstra-ted that agents (including caffeine, yohimbine, and carbon dioxide) with various biochemical properties exhibit a significantly greater likelihood of triggering panic episodes in patients diagnosed with PD compared to controls, and in some cases, relative to patients with other anxiety or mood disorders without panic attacks.³³ Although these findings were initially interpreted as evidence suggesting that panic is a disorder of pathological biological processes, it is now widely accepted that both biological and psychological processes are responsible for the etiology and persistence of this condition.

A number of neural systems have been implicated in the development and maintenance of panic, with a particular focus on central neurotransmitter systems (including norepinephrine, serotonin, and γ-aminobutyric acid [GABA]). Numerous studies support the role of noradrenergic mechanisms in the pathophysiology of PD, with particular importance placed on the locus coeruleus (LC), the primary source of the brain’s norepinephrine. Stimulation of the LC has been found to increase panic and anxiety in both animals and humans. Conversely, commonly used antipanic agents (such as benzodiazepines and antidepressants) have been found to block LC firing.³⁴

Disruptions in the serotonin system have also been implicated in the pathophysiology of PD. One study found that, compared to controls, individuals with PD demonstrated reduced serotonin transport binding in the midbrain, temporal lobe, and thalamus.³⁵ Additionally, selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and tricyclic antidepressants (TCAs), all of which have effects on serotonergic neurotransmission, have demonstrated efficacy in the amelioration of panic symptoms.³⁶

The widespread use of benzodiazepines in the treatment of PD has led many to hypothesize that GABA, an inhibitory neurotransmitter, is relevant to the underlying pathophysiology of this condition. Benzodiazepines increase GABA-ergic transmission and have demonstrated efficacy for PD. Consistent with these findings, people with PD display diminished benzodiazepine receptor sensitivity.³⁷ High densities of benzodiazepine-GABA receptors have been found in brain regions (most notably the amygdala and hippocampus) implicated in anxiety and fear responses.³⁸ Converging evidence comes from a neuroimaging study that reported reduced GABA levels in the occipital cortex of individuals with PD³⁹; interestingly, citalopram, an SSRI effective for a range of depressive and anxiety disorders (including PD), is associated with increases in GABA levels in the occipital cortex of healthy controls.⁴⁰

The limbic system, including most notably the amygdala, appears to be important in the neurobiology of panic. A critical role of the limbic system is to scan the environment for threat-relevant cues, in addition to monitoring interoceptive (bodily) sensations, and to integrate these diverse sources of information to assess the magnitude of threat and the need for action to achieve safety. Recent neurobiological findings have demonstrated that patients with PD have reduced amygdala volumes,⁴¹ as well as reduced cerebral glucose metabolism in the amygdala and hippocampus, along with thalamus and brainstem areas.⁴² In addition, decreased volume of the temporal lobe⁴³ and reduced creatine and phosphocreatine metabolites in the medial temporal lobe have been reported.⁴⁴ Finally, one recent study found that reduced orbitofrontal blood flow predicted panic response to the respiratory stimulant doxapram,⁴⁵ consistent with inhibitory action of this area on amygdala activity. In summary, current neurobiological research is now focused on perturbations of these fear networks in the brain, rather than on a single neurotransmitter or neurochemical explanation of the pathophysioiology underlying panic.

Psychopathological Processes

The psychological construct that has received the most attention in PD research is anxiety sensitivity, the belief that anxiety and its related symptoms may lead to deleterious physical, social, and psychological consequences (e.g., fainting, embarrassment, loss of control, “going crazy,” or death).⁴⁶ The empirical evidence demonstrates that anxiety sensitivity predicts the onset of panic attacks in a variety of samples (including adolescents, college students, and the general population).⁴⁷ The origins of anxiety sensitivity are not fully understood, and it is unclear what role genetics and biology play in its development. Some experiential contributions to the development of anxiety sensitivity likely include repeated exposure to aversive experiences (e.g., a personal history of illness or injury), vicarious observations (e.g., significant illnesses or death among family members), informational learning (e.g., repeated warning messages from parents), parental reinforcement of attention to somatic symptoms, parental modeling of distress in response to bodily sensations, and the occurrence of panic attacks themselves.⁴⁸

Anxiety sensitivity is posited to maintain panic through two mechanisms. First, it has been argued that panic attacks may become conditioned to themselves, as a conditioned fear of internal cues (i.e., interoceptive conditioning). According to this account, early physical sensations of the anxiety response elicit subsequent intense bursts of anxiety or panic due to previous pairings with the experience of panic.⁴⁹ These models offer one psychological explanation for the unexpected nature of panic. Cognitive-behavioral formulations, on the other hand, suggest that catastrophic misinterpretation of bodily sensations is the core factor responsible for the maintenance of PD.⁵⁰ Common misappraisals include the fear that bodily sensations are a sign of imminent death (e.g., heart attack or suffocation), loss of control (e.g., going crazy or fainting), or social catastrophe (e.g., embarrassment or humiliation). In turn, those misinterpretations heighten anxiety (and the associated physical sensations), which triggers further misappraisals. Although many patients can identify particular feared consequences associated with their panic, they may not be aware of specific catastrophic misappraisals in the exact moment of a panic episode, suggesting that misappraisals themselves may also become conditioned stimuli that trigger panic outside of one’s conscious awareness. According to both accounts, following an initial exposure to panic, a “fear of fear” develops (i.e., fear of physical sensations associated with a normal fear response), wherein exposure to either physical or cognitive cues associated with prior panic will provoke a state of panic. While anxiety sensitivity was initially conceptualized as a trait, it has become clear that anxiety sensitivity itself may be reduced both with cognitive-behavioral and pharmacological interventions.

SOCIAL ANXIETY DISORDER

Although clinical descriptions of social phobia appeared some 40 or more years ago,⁵¹ social phobia did not appear as a unique diagnostic entity until the DSM-III was published in 1980. Originally conceptualized as a “phobic disorder,” definitions of social phobia were restricted to specific performance-related situations (e.g., public speaking), while fear of social interaction situations was absent in this early diagnostic nomenclature. The definition of social phobia expanded with the revision of the DSM-III in 1987, and included both performance and social interaction situations. Presently, social phobia, or social anxiety disorder (SAD), is recognized as a prevalent and often incapacitating anxiety disorder characterized by a marked and persistent fear of one or more social or performance situations in which the person is exposed to unfamiliar people or to possible scrutiny by others.⁵² Although once referred to as “a neglected anxiety disorder,”⁵³ the past two decades have witnessed a burgeoning of empirical research dedicated to better understanding the psychology and neurobiology of social fears and anxiety.

Clinical Characteristics and Diagnosis

The fundamental characteristic of SAD is a marked and persistent fear of situations that involve performance, evaluation, or potential scrutiny by others.⁵² People with SAD fear that they will act in way or show anxiety symptoms that will be embarrassing or humiliating, or that may result in negative evaluation by others. Consequently, the feared social interaction or performance situations are avoided or else endured with intense distress and anxiety (see Table 32-4 for DSM-IV diagnostic criteria). Commonly feared or avoided situations may include attending parties or social gatherings, meeting new people, initiating or maintaining conversations, participating in group meetings, being the center of attention, interacting with authority figures, being assertive, speaking in public, and eating or drinking in public. Patients often report significant anxiety in anticipation of feared social events, and may report panic attacks on exposure to such situations.

Table 32-4 DSM-IV Criteria for Social Phobia

• A marked and persistent fear of one or more social or performance situations in which the person is exposed to unfamiliar people or to possible scrutiny by others. The individual fears that he or she will act in a way (or show anxiety symptoms) that will be humiliating or embarrassing. NOTE: In children, there must be evidence of the capacity for age-appropriate social relationships with familiar people and the anxiety must occur in peer settings, not just in interactions with adults.

• Exposure to the feared social situation almost invariably provokes anxiety, which may take the form of a situationally bound or situationally predisposed panic attack. NOTE: In children, the anxiety may be expressed by crying, tantrums, freezing, or shrinking from social situations with unfamiliar people.

• The person recognizes that the fear is excessive or unreasonable. NOTE: In children, this feature may be absent.

• The feared social or performance situations are avoided or else are endured with intense anxiety or distress.

• The avoidance, anxious anticipation, or distress in the feared social or performance situation(s) interferes significantly with the person’s normal routine, occupational (academic) function, or social activities or relationships, or there is marked distress about having the phobia.

• For individuals under age 18 years, the duration is at least 6 months.

• The fear or avoidance is not due to the direct physiological effects of a substance (e.g., a drug of abuse or a medication) or a general medical condition and is not better accounted for by another mental disorder.

• If a general medical condition or another mental disorder is present, the fear of a performance situation is unrelated to it.

The DSM-IV recognizes two distinct subtypes of SAD: generalized and nongeneralized (or circumscribed). The nongeneralized subtype is generally limited to public speaking or to other performance situations, and consequently is often less disabling, although it may result in impairment at work or school.⁵⁴ In contrast, generalized SAD is associated with greater impairment because the anxiety is pervasive and occurs in many social and performance situations. Individuals with generalized SAD often fear and avoid both social interaction situations (e.g., social gatherings and meeting new people) and performance situations (e.g., public speaking).

Epidemiology

SAD is a common psychiatric condition, with lifetime prevalence rates in Western countries ranging between 7% and 13%.⁵⁵ Variations in prevalence rates depend on diagnostic criteria (i.e., DSM-III, DSM-III-R, or DSM-IV), diagnostic threshold (e.g., required level of distress or impairment necessary to meet diagnostic criteria), and method of assessment (e.g., self-report surveys or interviews). Results from the recent National Comorbidity Survey—Replication (NCS-R) indicate that SAD occurs at a lifetime prevalence of approximately 12.1% in the general population, making it the fourth most prevalent psychiatric disorder, behind MDD, alcohol dependence, and specific phobia.⁶ Earlier work based on comparable population estimates found that the generalized subtype occurs in about two-thirds of people diagnosed with SAD, with the nongeneralized subtype present in one-third.⁵⁶

SAD is more common in women than in men, with a ratio of about 3:2. However, in individuals who seek treatment, men and women are equally represented. Some have argued that this disparity is the result of differential social expectations, gender roles, or differing levels of distress, with symptoms causing more impairment for men than women.⁵⁷ Gender, however, does not appear to influence age of onset, duration of illness, or co-morbidity.⁵⁸^–⁶⁰ Research conducted within the United States has failed to find significant differences in race or ethnicity in SAD within the general population.⁶¹ In some cases, however, prevalence rates have been shown to differ markedly between countries. For example, Asian communities report the lowest lifetime prevalence rates (less than 1%) of SAD.⁵⁵

SAD typically has an early age of onset, surfacing in either childhood or adolescence, and often persists well into adulthood following a chronic, unremitting course that significantly interferes with the afflicted individual’s life.⁶² Although the average age of onset of SAD appears to be around 16 years of age,⁶¹ many patients report being shy or socially anxious since early childhood. Empirical evidence suggests that people with SAD have a mean duration of illness of around 25 years when they seek treatment and low rates of spontaneous recovery.⁶³ Those striking facts illustrate that for many, SAD is a life-long illness, and highlight the vast underutilization of treatment services for this common and debilitating condition.

Impairment and Quality of Life

Functional impairment is common in people with SAD. This condition is associated with educational and occupational underachievement, impaired social relationships, social isolation, and an overall diminished quality of life.⁶⁴ Afflicted individuals tend to be less well educated and of lower socioeconomic status compared to people in the general population. Work impairment is also common, with research showing that people with SAD are twice as likely to report at least one disability day in a given 2-week period compared to people without SAD. Evidence also shows that people with SAD report greater physical health–related problems and physical impairment. The presence of co-morbid psychiatric conditions greatly increases the impairment and disability related to SAD. In terms of social function, socially anxious individuals have been found to have fewer friends, and are less likely to date or to marry compared to people in the general population, as well as relative to patients with other anxiety disorders.^64,⁶⁵ Interestingly, even when people with social anxiety do develop friendships and intimate relationships, they often view those relationships as less functional and satisfying than do people without social anxiety.^66,⁶⁷

Co-morbidity

SAD is highly co-morbid with other psychiatric illnesses. For instance, results from the initial National Comorbidity Survey (NCS) found that 81% of people with SAD met criteria for at least one other lifetime DSM-III-R psychiatric diagnosis; 19% reported one other disorder, 14% reported two other disorders, and 48% reported three other disorders.⁶¹ Not surprisingly, individuals with the generalized subtype of SAD are more likely to suffer from co-morbid mood and anxiety disorders than individuals with the nongeneralized subtype.⁶⁸ It is particularly notable that the onset of SAD often appears to precede the onset of other co-morbid disorders, suggesting that SAD may be a risk factor for the development of other psychopathology.^60,⁶¹

Anxiety disorders are the most commonly reported co-morbid illness, with 57% of people with SAD endorsing criteria for at least one other anxiety-related condition. Data from the NCS revealed the presence of PTSD in 16% of individuals with SAD, in 11% of those with PD, and in 13% of those with GAD.⁶¹ In treatment-seeking populations, the rates of co-morbid anxiety disorders are often higher, with rates of co-morbid SAD reported near 45% in primary PD samples.⁶⁹ In primary social phobia, co-morbid GAD has been reported in 24%.⁷⁰ Some evidence suggests that in some cases SAD may occur secondarily to trauma or to PTSD.⁷¹

SAD has also been shown to be highly co-morbid with the spectrum of mood disorders. In the NCS, secondary MDD was present in 37% of those with SAD.⁷² Lifetime rates of co-morbid MDD in clinical samples have been reported near 60%.⁷³ Individuals with SAD appear to be at significant risk for the later development of depression, in light of evidence demonstrating that onset of SAD typically occurs many years before the onset of depression.⁵⁹ In a longitudinal investigation, participants with SAD and depression in adolescence or early adulthood were found to be at greatest risk for subsequent depression, and displayed greater susceptibility to a more difficult course of illness.⁷⁴ Research also demonstrates that individuals with SAD are at increased risk of suicidal ideation⁶⁰ and have an increased rate of suicide attempts⁷⁵ compared to those in the general population. Finally, recent evidence suggests that rates of bipolar disorder may also be elevated in people with SAD. In a recent multicenter study of patients with bipolar I or II disorder, lifetimes rates of SAD were 22%, which is greater than prevalence rates reported in general community samples.⁷⁶