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date: 18 April 2019

Overview and Introduction to Anxiety Disorders

Abstract and Keywords

This chapter provides an overview of the Oxford Handbook of Anxiety and Related Disorders, and an introduction to the nature and treatment of anxiety and related disorders. With 51 chapters, this handbook covers a wide range of topics related to anxiety disorders, including phenomenology, etiology, assessment, and treatment. Key features of panic attacks and of each of the major anxiety disorders (e.g., panic disorder and agoraphobia, social phobia, specific phobia, generalized anxiety disorder, obsessive-compulsive disorder, and posttraumatic stress disorder) are reviewed. Etiological factors such as genetics, biological processes, learning, information processing, cultural factors, and personality are considered. The chapter concludes with a review of effective treatments (e.g., pharmacotherapy, psychological interventions, and combined approaches).

Keywords: anxiety disorders, etiology, treatment

Orientation to the Handbook

As the fields of psychology, psychiatry, and related disciplines evolve, it is important for researchers and clinicians to remain up-to-date with the latest empirical findings, theoretical perspectives, and trends that subsequently guide their practices. In the area of anxiety research, significant gains have been made in recent years with respect to our conceptualization of anxiety disorders and the development of evidence-based treatments. While traditional theories and approaches remain highly influential, health professionals are continually searching for strategies and interventions to enhance existing therapies.

The primary goal in developing this text was to create a comprehensive and up-to-date handbook that would detail the various research and clinical developments in the field of anxiety. From phenomenology and classification to treatment and comorbidity, the reader is provided with extensive descriptive information, empirical findings, areas of controversy, and suggested future directions.

The balance between breadth and depth and the integration of both traditional and contemporary theories will appeal to clinicians, researchers, educators, and students alike. Each topic was chosen to reflect clinical and theoretical approaches that currently inform our understanding of the development and treatment of anxiety disorders. Furthermore, in order to incorporate multiple approaches and perspectives, chapters were written by authors from a variety of academic disciplines and clinical backgrounds (e.g., psychology, psychiatry, nursing, social work).

The first part of the book includes this overview and introduction. Part Two provides a descriptive review of each of the main anxiety disorders: panic disorder, social phobia, and specific phobia (Chapter 3), generalized anxiety disorder (GAD) (Chapter 4), obsessive-compulsive disorder (OCD) (Chapter 5), and posttraumatic stress disorder (PTSD) (Chapter 6). In addition to a review of diagnostic criteria, prevalence rates, and comorbidity, each chapter highlights current (p. 4) conceptual, methodological, and clinical issues in the field. For example, suicide risk, health care utilization, and functional impairment across the anxiety disorders are discussed in Chapter 2. Hazlett-Stevens, Pruitt, and Collins (Chapter 4) add clarity to the term worry in GAD by differentiating it from obsessive thoughts, depressive ruminations, and “normal” levels of worry in the general population. In her review of OCD, Mathews (Chapter 5) discusses the pros and cons of various subtyping approaches and highlights current diagnostic and conceptual issues between OCD and other comorbid conditions.

Part Three focuses on empirically supported neurobiological and psychological approaches to understanding anxiety disorders. Chapters 7 through 10 describe advances in animal research (Chapter 7), genetic research (Chapter 8), and neuoranatomical models (Chapter 9) that have contributed to our evolving understanding of the biological processes involved in decision making, detection of threat, and emotional responding. Chapters 11 through 19 offer detailed descriptions of the most influential psychological models in the field of anxiety. While some chapters provide details on well-established theoretical models (e.g., learning theories, cognitive behavioral models), other chapters present more contemporary and integrative theories (e.g., Barlow's “triple vulnerability” model in Chapter 13; emotional dysregulation and intolerance of uncertainty models of GAD in Chapter 17). This section is strengthened by the addition of several chapters that focus on developmental theories, early prevention (Chapter 11), the impact of family and social relationships (Chapter 14), and the role of personality (Chapter 15) in the development and maintenance of anxiety disorders.

Part Four presents current issues in classification and assessment. Establishing accurate diagnoses, determining predominant conditions, and ruling out additional disorders is a challenging and complex skill. Given that diagnoses have important implications for case conceptualization and treatment planning, a thorough and up-to-date understanding of issues that may complicate assessment (e.g., differential diagnoses, comorbidity) is essential. Lawrence and Brown (Chapter 20) address concerns regarding diagnostic overlap between syndromes and draw attention to the limitations of the primarily categorical approach adopted in the current edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM–IV–TR; American Psychiatric Association [APA], 2000). The following chapter on assessment strategies (Chapter 21) reviews the functions of assessment and provides a useful framework for selecting various empirically supported assessment measures.

Part Five represents the largest section of this book and focuses specifically on treatment approaches. For each of the major anxiety disorders, detailed discussions of both pharmacological and psychological approaches are provided. In addition to reviewing empirical data on traditional and well-recognized interventions, these chapters also highlight innovative and alternative treatment approaches. For example, chapters include information on the use of virtual reality (Chapter 25), transdiagnostic protocols (Chapter 33), the use of herbal products and complementary treatments (Chapter 34), acceptance and mindfulness-based approaches (Chapter 36), and self-help treatments (Chapter 37). In addition, unique issues such as treating nocturnal panic attacks (Chapter 22), eye movement desensitization reprocessing techniques in PTSD (Chapter 31), the use of surgical procedures to treat OCD (Chapter 28), prevention of anxiety in children (Chapter 38), and treating anxiety in primary care settings (Chapter 39) are also discussed in detail.

The attention to breadth and depth is also apparent in the next three sections of the book where in-depth information is provided about other anxiety-based conditions, (e.g., hypochondriasis, body dysmorphic disorder), special topics related to comorbid substance use, cultural issues, and the impact of anxiety disorders in specific populations (e.g., children, older adults). Additionally, the inclusion of such topics as the fear of pain (Chapter 42) and the relationship between anxiety and sleep (Chapter 47) further expand our scope of understanding. The final part of the book (Chapter 51) provides an overview of future directions in anxiety disorders research.

In the remainder to this introductory chapter, a brief introduction to the diagnostic features of the anxiety disorders will be provided, followed by a general summary of issues pertaining to etiology and treatment. The purpose of this section is to offer a concise review of the major themes, concepts, and approaches that will be discussed in subsequent chapters.

General Introduction to the Anxiety Disorders

The anxiety disorders are among the most common and debilitating of the psychological disorders. Often chronic in nature, anxiety disorders are associated with severe impairments across interpersonal (p. 5) and occupational domains. The purpose of this section is to provide a general introduction to the main anxiety disorders outlined in the DSM–IV–TR. Specific attention is given to diagnostic features, prevalence rates, comorbidity, and issues in assessment.

Panic Attacks

The DSM–IV–TR defines a panic attack as a period of intense fear or discomfort in which the individual experiences at least four of the following symptoms (peaking in intensity within 10 minutes or less): racing or pounding heart, sweating, trembling, shortness of breath, choking sensations, chest pain or tightness, nausea or stomach upset, dizziness, derealization or depersonalization, fear of losing control or going crazy, fear of dying, numbness or tingling sensations, and chills or hot flushes. The term limited symptom attack is used to describe an attack in which fewer than four symptoms are present. Panic attacks are not specific to any one anxiety disorder. For example, individuals with panic disorder, specific phobia, and social phobia may experience panic attacks during the course of their illness. In order to provide greater diagnostic and descriptive clarity, there are three main types of panic attacks. Unexpected or “uncued” attacks are those that occur in situations or places in which the individual normally feels safe. Often, people report that they occur “out of the blue” and are not associated with any specific trigger or cue. Situationally bound or “cued” attacks are those that occur almost always in response to a feared stimulus (e.g., a person with a specific phobia of driving experiences a panic attack when riding in a car). Situationally predisposed attacks are those that are more likely to occur in particular types of situations, but do not always occur (e.g., a person with panic disorder with agoraphobia who often has panic attacks in public places).

Panic Disorder

Diagnostic criteria for panic disorder require that an individual experience recurrent and unexpected panic attacks that are followed by a period of at least 1 month of marked worry about having additional attacks, anxiety about the implications of the attacks (e.g., having a heart attack, going crazy), and/ or a significant change in behavior. Although they frequently co-occur, panic disorder may or may not be associated with agoraphobia, or the intentional avoidance of situations/places from which it might be difficult to escape or receive help in the event of a panic attack (e.g., being away from home, crowds, public transportation, shopping malls). For individuals whose symptoms have never met full criteria for panic disorder but who endorse significant avoidance and fear of panic-like symptoms (e.g., diarrhea, dizziness), a diagnosis of agoraphobia without a history of panic disorder may be warranted. Lifetime prevalence rates of panic disorder (with or without agoraphobia) in the general population are estimated to be at about 4.5%, whereas agoraphobia without history of panic disorder has been found to occur in 1.4% of the population (Kessler, Berglund, Demler, Jin, & Walters, 2005). This condition is more common among women than men. Symptoms typically develop in late adolescence or early adulthood and tend to vary in frequency and intensity across the lifespan.

Social Phobia

The essential feature of social phobia (or social anxiety disorder) is marked fear and anxiety about being negatively evaluated in social or performance-based situations (e.g., public speaking, meeting strangers, maintaining conversations). Fearful of being judged, criticized, or embarrassed, individuals with social phobia often avoid social situations or endure them with considerable distress. For individuals whose fears are related to multiple situations (e.g., formal speaking, eating in front of others, dating situations, etc.), the diagnostic specifier generalized type may be added. Common in the general population (lifetime prevalence rates range from 7% to 13%) (Furmark, 2002;Ruscio et al., 2008), the disorder typically begins in early adolescence (APA, 2000). In addition, it is not uncommon for social phobia to be associated with substance use, bulimia nervosa, and to occur within the context of a mood disorder or other anxiety disorders. Currently, an area of debate and an issue of diagnostic specificity is the significant symptom overlap between social phobia on Axis I and avoidant personality disorder on Axis II (see Chapter 3).

Specific Phobia

The DSM–IV–TR describes specific phobia as clinically significant anxiety and disproportionate fear of specific objects or situations. The five main types of specific phobia in DSM–IV–TR include animal type (e.g., fear of snakes, spiders, dogs), natural environment type (e.g., fear of heights, storms, water), blood-injection-injury type (e.g., fear of blood, needles, surgery), situational type (e.g., fear of enclosed places, driving, flying), and other (p. 6) type (e.g., fear of vomiting, choking, or other specific objects or situations). Despite awareness that their fear is excessive, individuals with specific phobia typically avoid the feared object or situation. Although specific phobia is among the most commonly occurring anxiety disorders, with a recent lifetime prevalence estimate of 12.5% (Kessler et al., 2005), only a small proportion of sufferers (12% to 30%) are estimated to seek treatment for their symptoms (APA, 2000). Often, specific phobias are diagnosed as additional disorders in people suffering from other anxiety disorders or depression. In these cases, the other disorder is usually the prominent focus of attention. Among the anxiety disorders, specific phobias are the most responsive to treatment. As discussed in greater detail in Chapter 25, significant improvements have been observed after a single session of exposure treatment. With regard to assessment, it is important for clinicians to be aware of diagnostic similarities between specific phobia and other psychological disorders such as hypochondriasis (fear of illness or disease), panic disorder (fear of physical sensations), and eating disorders (fear of food or weight gain).

Obsessive-Compulsive Disorder

Obsessive-compulsive disorder (OCD) is characterized by persistent and intrusive obsessions and/or compulsive behaviors. Obsessions may take the form of thoughts, images, or impulses and often surround themes such as contamination, doubting, aggression, accidental harm, religion, or thoughts of a sexual nature. Unlike a delusional or psychotic disorder, individuals with OCD recognize that their obsessions are a product of their own mind (APA, 2000). Compulsions are ritualistic behaviors that an individual feels compelled to perform in order to reduce feelings of anxiety and discomfort brought on by the obsession. Compulsive behaviors may include repeated hand-washing, checking, counting, hoarding, or a need for symmetry. In order to meet diagnostic criteria for OCD, the obsessions and compulsions must either be time-consuming or cause clinically significant distress. Prevalence rates for OCD have been estimated to be approximately 1.6% in community samples (Kessler et al., 2005) and the disorder appears to be about equally distributed among males and females (APA, 2000). Accurate assessment of OCD is complicated by the need to differentiate obsessions from delusional beliefs, depressive ruminations in major depressive disorder, and excessive worries about real-world concerns in generalized anxiety disorder (see Chapter 4). A key area of current interest among researchers and clinicians is the relationship between OCD and disorders that have similar obsessive and compulsive traits. Sometimes referred to as the obsessive-compulsive spectrum disorders, some researchers hypothesize that conditions such as Tourette's syndrome, body dysmorphic disorder, trichotillomania, eating disorders, hypochondriasis, and obsessive-compulsive personality disorder may be etiologically similar to OCD.

Posttraumatic Stress Disorder

Posttraumatic stress disorder (PTSD) describes a set of characteristic somatic and cognitive symptoms, lasting at least 1 month, that occur in response to a highly traumatic event. As outlined in the DSM–IV–TR, the individual must experience or witness a traumatic event involving physical threat to the self or other (e.g., serious car accident, rape, combat). The criteria also specify that the person's response to the event must be one of intense fear, helplessness, or horror. In addition, individuals must demonstrate clinically significant and distressing symptoms from three distinct clusters: reexperiencing symptoms (e.g., recurrent nightmares, intrusive thoughts, flashbacks), increased arousal (e.g., irritability, hypervigilance), and avoidance/numbing symptoms (e.g., feelings of detachment, avoidance of people or places connected to the trauma). Posttraumatic stress disorder can be acute (〉 3 months duration), chronic (〈 3 months duration), or with delayed onset (symptoms develop 6 months after traumatic event). In the general population, PTSD has a lifetime prevalence rate of approximately 8% (APA, 2000); however, rates are significantly greater among victims of abuse, crime, and war. Chapter 6 provides a review of epidemiological data, risk factors, and prominent psychological models of PTSD.

Acute Stress Disorder

Introduced with the publication of DSM-IV (APA,1994), acute stress disorder (ASD) is a relatively new diagnostic entity. The term is used to describe the development following exposure to a traumatic event of time-limited symptoms that are similar to those in PTSD (e.g., reexperiencing, avoidant, and arousal symptoms). However, ASD differs from PTSD in that it must occur within 1 month of the traumatic event and may not last longer than 4 consecutive weeks (beyond which a diagnosis of PTSD might be made). In addition, there is greater emphasis on dissociative symptoms (p. 7) in ASD (e.g., depersonalization, numbing, derealization, dissociative amnesia). The exact prevalence of ASD is not presently known, although estimates ranging from 14% to 33% in the aftermath of traumatic events have been described in the literature (APA, 2000). For more information on ASD and other stress-based responses (e.g., complex PTSD, disorders of extreme stress), see Chapter 6.

Generalized Anxiety Disorder

The hallmark of generalized anxiety disorder (GAD) is excessive and pervasive worry about a variety of topics such as minor matters (e.g., punctuality, small repairs), job security, finances, health of loved ones, future events. Worries in GAD are distinguished from nonpathological worry by their unrealistic and uncontrollable nature. In GAD, the worry is frequent (occurring more days than not) and chronic (lasting at least 6 months), though individuals with GAD often report that they have worried in this manner for the majority of their life. The criteria for GAD also require that individuals report at least three of the following symptoms: restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and difficulty sleeping. Lifetime prevalence rates for GAD have been estimated to be 5.7% (Kessler et al., 2005), and GAD is more common among women than men (APA, 2000). Similar to the patterns observed in other anxiety disorders, individuals with GAD often have additional psychological disorders, the two most common being major depressive disorder and panic disorder (Campbell & Brown, 2002). More information about the features of GAD can be found in Chapter 4. It is also notable that, as GAD has evolved diagnostically over the past two decades, pharmacological and psychological treatments for GAD have also advanced. A review of the empirical data and a discussion on more contemporary approaches to treatment are described in Chapters 26 and 27.

Etiology of Anxiety Disorders

Most theorists agree that a single etiological cause in not sufficient to explain the developmental complexity and heterogeneity that characterize the anxiety disorders. Whereas early theoretical accounts tended to emphasize the independent and exclusive role of either nature (e.g., biology, including genetics) or nurture (e.g., learning, environment), contemporary theories of the development and maintenance of anxiety are based on more sophisticated, biopsychosocial models that include cognitive, behavioral, genetic, and environmental elements. Over the past 20 years, these multidimensional approaches have greatly enhanced the way clinicians understand and treat these disorders. The following section will provide a brief introduction to the predominate approaches that currently guide research and treatment protocols.

Biological Processes

A great many biological processes have been implicated in risk for anxiety disorders, as well as in expression of anxiety disorders. In the past decade, biochemical theories of anxiety—which, it should be noted, overlap substantially with biochemical theories of depression—have focused on neurotransmitter systems that use serotonin (5-HT) or corticotropin-releasing factor (CRF), though numerous other neurotransmitters and neurohormones have also been implicated (see Chapters 7 and 10). More recently, there has been some convergence of theory (and supporting evidence) that risk for many (though perhaps not all of the) anxiety disorders may overlap substantially with biological factors that influence anxiety-related personality traits (e.g., the confluence of high neurosis and low extraversion, sometimes referred to as “neurotic introversion”) (Bienvenu, Hettema, Neale, Prescott, & Kendler, 2007). What types of biological factors fit this mold?

There is evidence from animal studies that variation in the serotonin transporter promoter (5-HTTLPR) is relevant to our understanding of the relationship between personality and anxiety (and depressive) disorders. Mice with loss of serotonin transporter function due to genetic knockout have increased anxiety-like behaviors and exaggerated stress responses (Holmes, Murphy, & Crawley, 2003). In addition, Barr et al. 2004 assessed stress responsivity in infant rhesus macaques reared either with their mothers or in peer-only groups. At 6 months of age, adrenocorticotropic hormone (ACTH) responses and cortisol levels were measured at baseline and during a period of separation. Serotonin transporter genotype was also measured, and animals were characterized as either being homozygous for the long form of the serotonin transporter (“l/l”) or having one copy of the long form and one copy of the short form (“l/s”). It was found that ACTH and cortisol levels increased during separation, consistent with the stressful nature of this experience. There was also an interaction between rearing experience and 5-HTLLPR genotype such that l/s animals had higher ACTH levels during separation than did l/l animals. This study is an (p. 8) example in nonhuman primates of how early life experience and genetics may interact to yield alterations in stress responsiveness and, by inference, risk for anxiety and mood disorders. The observation—now oft-replicated—that human variation in this polymorphism (5-HTTLPR) is associated with risk for adverse mental health outcomes (e.g., depression) in the context of life stress has resulted in 5-HTTLPR becoming the gene celebre of anxiety and depression research. More important, however, it has taken discussion of biopsychosocial models from the realm of the philosophical to the level of systems neuroscience (Caspi & Moffitt, 2006), ushering in an era of testable theories about genes and environment and their interaction. Though much of this work to date has focused on gene-environment interactions relevant to understanding depression, evidence is accruing that these relationships may be equally—or more—important for understanding risk for anxiety and related disorders (Stein, Schork, & Gelernter, in press). The role of genetic factors in anxiety and related disorders is covered in Chapter 8.

The notion of differential susceptibility to stress is certain to influence our thinking about the etiology of anxiety for years to come. In fact, measures of psychological resilience have been developed and validated (Campbell-Sills & Stein, in press; Connor & Davidson, 2003), and are likely to feature more prominently in research studies. Furthermore, the concept of resilience to stress is now being considered from a neuroscience perspective, yielding many candidate systems—above and beyond those involving serotonin—whose further study will undoubtedly help us ascertain individual differences that determine how the human psyche can so often thrive in the face of great adversity (Charney, 2004).

Brain imaging has provided another window into the biology of anxiety and related disorders, and is the focus of Chapter 9. Having evolved from studies of symptom provocation to the use of various types of emotion-processing tasks (e.g., the viewing of emotional faces), investigators have identified neural circuits that seem to function differently in patients with anxiety disorders. Two brain regions that have been consistently observed in patients with anxiety disorders to exhibit increased responsiveness in these types of paradigms are the amygdala and insula (Etkin & Wager, 2007). Moreover, hyperactivity in these regions has also been seen in individuals with high levels of traits such as neuroticism or anxiety sensitivity that can be considered to characterize them as anxiety-prone (Stein, Simmons, Feinstein, & Paulus, 2007), therein extending the possibility that this represents a “core” biological feature of these disorders. Notably, however, not all anxiety disorders share all these functional neuroimaging features (e.g., OCD), and it is these differences that may ultimately support the kind of biologically based classification system discussed earlier in this chapter.

Psychological Processes

Psychological theories of anxiety have predominately focused on the role of cognitive processes and behavioral responses to describe the acquisition and maintenance of anxiety disorders. Behavioral models include both classical and operant conditioning theories, highlighting the role of learning and the reinforcing nature of maladaptive responses to objects or situations. Classical conditioning models posit that fear and phobias develop as a result of the pairing between a neutral stimulus (e.g., dog) and an aversive experience (e.g., being bitten by a dog). While this model offered insight into the etiology of anxiety disorders, it did not account for the persistence and generalization of the fear response (e.g., fearing all dogs). To address this shortcoming, Mowrer 1960 proposed a two-factor theory of fear acquisition. Drawing from the pioneering work of Pavlov, Watson, and Skinner, he theorized that fears were established through principles of classical conditioning and maintained as a function of operant conditioning. In other words, while the avoidant and escape behaviors commonly observed among anxiety sufferers reduce distress and suffering in the short-term, they ultimately perpetuate anxiety in the long-term through negative reinforcement. In this way, the natural course of extinction is prevented and the fear is maintained. Several chapters include information on the influence of traditional and present-day learning theories among the anxiety disorders including posttraumatic stress disorder (Chapter 19), panic and phobias (Chapter 16), and generalized anxiety disorder (Chapter 17).

While conditioning models were highly influential, several important limitations were identified. For instance, they are unable to explain why some people develop phobias and others do not, after exposure to the same aversive or distressing stimulus. They also fail to explain how some individuals develop anxiety disorders in the absence of a personally aversive experience (e.g., developing a fear of flying, without having ever been on a plane). It was also unclear why certain stimuli (e.g., snakes, spiders, (p. 9) heights) were more likely to establish a fear response than others (e.g., electrical outlets, guns). The criticisms concerning the behavioral theories prompted clinicians and researchers to develop more sophisticated and inclusive models to explain anxiety, and to acknowledge the importance of observational learning, learning through the verbal transmission of information, emotional processing, and biological constraints on learning (e.g., Craske, Hermans & Vansteenwegen, 2006; Otto, 2002; Rachman, 1976; Rothbaum, 2006).

Some of the most influential work to emerge in the field of anxiety disorders was based on cognitive theories and approaches. Beck's (1976) cognitive theory of anxiety and depression was particularly important in providing a conceptual framework for anxiety. He proposed that emotions were largely determined by dysfunctional thoughts, beliefs, and attitudes. For example, a person with social phobia may believe that he or she will be ridiculed and rejected by others and consequently begins to experience anxiety and fear. In turn, these beliefs lead to avoidant behaviors, which, as previously noted, serve to maintain fear by prohibiting the individual from learning how to successfully cope with an anxiety-provoking situation. In addition, research has shown that maladaptive thoughts and beliefs significantly impact other cognitive domains such as memory, attention, and information processing. For instance, individuals with anxiety disorders are more likely to selectively recall and attend to fear-congruent objects or situations in their environments, and to process ambiguous stimuli as threatening (Mathews & MacLeod, 1994). McNally and Reese (Chapter 12) provide a comprehensive review of this area.

The specific meanings that people attach to their thoughts and experiences have also received increased attention in recent years. David Clark's 1986 influential theory proposed that one of the key variables that determined the maintenance of panic disorder was the misinterpretation of physical sensations (see Chapter 16). For example, a person with panic disorder may sense uncomfortable physical sensations during a panic attack (e.g., increased heart rate, shaking) and interpret these sensations as a sign of impending danger (“I'm having a heart attack”; “I will die or lose control if this continues”). Also drawing from the cognitive theories, Paul Salkovskis (2002) has emphasized the role of beliefs about personal responsibility and a sense of inflated importance that individuals with OCD attribute to their obsessional thoughts (see Chapter 18). Concepts such as thought-action fusion (e.g., believing that having a thought increases the likelihood of a particular outcome) and the tendency for individuals with OCD to believe that their intrusive and disturbing thoughts are a reflection of their underlying moral character are additional examples of how beliefs and perceptions shape and maintain anxiety (see Chapter 18).

Developmental Processes

Developmental theories that contribute to current understandings of the anxiety disorders emphasize the role of childhood temperament, parenting styles, family relationships, and aversive experiences in early childhood. As outlined by Hudson and Rapee (Chapter 14), one area that has received much attention is the impact of parenting styles on the development and maintenance of anxiety. Research has fairly consistently demonstrated a strong relationship between the development of an anxiety disorder and parents who are described as controlling, and overprotective. Furthermore, anxiety disorders are more common among o spring of parents who support avoidant behaviors and who fail to adequately encourage independence in their children. Though more research is needed, there may be a relationship between anxiety disorders and parents who exhibit greater levels of rejection and indifference toward their children. With regard to the broader family in general, the degree of cohesion, warmth, and support between parents, children, and among siblings appears to increase risk for developing an anxiety disorder. The consequences of these factors on parent-child attachment are discussed in greater detail in Chapter 14.

In addition to these findings, it is also widely acknowledged that childhood temperament likely plays a significant role in the parent-child relationship. For instance, children who are shy, inhibited, anxious, or depressed may elicit overprotective behaviors in parents. Researchers have suggested that such parenting styles tend to increase a child's overall vulnerability to anxiety disorders by decreasing self-confidence, self-efficacy, and autonomy. Childhood temperament has also been associated with the development of specific anxiety disorders. In Chapter 11, Poulton, Grisham, and Andrews review research demonstrating a relationship between childhood hyperactivity, antisocial behavior, trauma exposure, and the subsequent development of PTSD. These data suggest that difficulties with emotion regulation in childhood may increase vulnerability to posttraumatic stress reactions as the individual may not be able to adequately process, (p. 10) integrate, and psychologically cope with aversive or traumatic experiences over his or her lifetime. Other types of aversive childhood experiences that tend to increase the risk of developing anxiety disorders include marital conflict and divorce, death of a parent, sexual abuse, mental health problems within the immediate family, and other psychosocial stressors such as financial strain and low socioeconomic status (for more information on these topics, see Chapters 11, 14, and 49).

Other prominent areas of study within the developmental framework include the evaluation of parental and extrafamilial modeling and the role of social and peer relationships. With regard to the former, there is some evidence to suggest that anxiety-related information may be transmitted to children through the behaviors and beliefs of their parents or from individuals in their social environments (see Chapter 14). For example, anxious parents may directly or indirectly communicate and reinforce avoidant behaviors in their children as a result of their own fears and phobias. In terms of social relationships, researchers are beginning to focus more attention on the role of peer victimization, social acceptance, and the quality of friendships as important variables in both the development and maintenance of anxiety disorders. Hudson and Rapee (Chapter 14) discuss the impact of social rejection, teasing, and bullying on anxiety and also provide information on including family members in treatment.

Cultural Influences

Researchers from a variety of clinical, theoretical, and international backgrounds have begun to explore the way in which cultural variables influence the development and expression of anxiety disorders. To date, the majority of research in this area has focused on differences in the presentation and prevalence rates of pathological anxiety between Eastern and Western societies. These data demonstrate that the anxiety disorders appear to be represented relatively consistently across cultures, although their manifestations may be markedly different. For example, obsessional thoughts in individuals with OCD tend to be culturally relevant (e.g., thoughts of witchcraft versus thoughts of sexually abusing a child). Asmal and Stein (Chapter 50) discuss how anxiety disorders vary across cultures and discuss similarities between various “culture-bound” syndromes. Though research in this area is still in its infancy, investigators hypothesize that the religious beliefs, norms, gender expectations, and illness perceptions of the dominant culture greatly shape the presentation of the anxiety disorders. Hudson and Rapee (Chapter 14) also describe briefly how specific cultural beliefs may shape reported prevalence rates.

Personality Traits and Disorders

One of the ways researchers have attempted to differentiate and further understand the anxiety disorders has been to evaluate the presence of specific personality traits among sufferers. The most consistent finding to date is that neuroticism occurs frequently across anxiety disorders. Other factors, however, have emerged that have become differentially associated with specific anxiety presentations. Pagura, Cox, and Enns (Chapter 15) discuss the unique relationships between anxiety sensitivity and panic disorder, perfectionism and OCD, antisocial behaviors and PTSD, and shyness/self-criticism in social phobia.

With regard to specific Axis II comorbidity, cluster C disorders (anxious/avoidant type) are most common among individuals with anxiety disorders. Rates of avoidant personality disorder, dependent personality disorder, and obsessive-compulsive personality disorder are particularly high among patients with social phobia, panic disorder, and OCD, respectively. The co-occurrence of these disorders presents unique challenges in the domains of assessment and treatment. As reviewed by Brandes and Bienvenu (Chapter 45), comorbid personality and anxiety disorders are associated with a more protracted clinical course, greater impairment and distress, increased suicidal ideation or attempts, and an overall poor response to treatment. A current area of debate involves the significant overlap between the diagnostic criteria for social phobia and avoidant personality disorder. Sharing many key features, some argue that the two disorders essentially capture the same construct at varying levels of intensity and functional impairment, with avoidant personality disorder corresponding to a more severe variant of social phobia. Further discussion regarding categorical versus dimensional classification approaches can be found in Chapter 20.

While the precise nature of the relationship between personality and anxiety is unclear, competing theories have been proposed to explain how they might interact and influence one another. For example, some researchers argue that personality traits and temperament are inherent factors that place an individual at greater risk for the subsequent development of an anxiety disorder. Others contend that the presence of chronic anxiety precedes and (p. 11) shapes the expression of specific personality traits. Still others propose that the co-occurring disorders share a common underlying cause and are, therefore, etiologically related. Relevant empirical data for these theoretical models and related treatment implications are presented in Chapter 45.

Treatment of Anxiety and Related Disorders

In recent years, a number of practice guidelines have been published on the treatment of anxiety disorders. These include guidelines from the Canadian Psychiatric Association on the treatment of all anxiety disorders (Swinson et al., 2006), as well as practice guidelines from the American Psychiatric Association on the treatment of particular anxiety disorders, including ASD and PTSD (APA, 2004), OCD (APA, 2007), and panic disorder (APA, 1998; Campbell-Sills & Stein, 2006) (note that the American Psychiatric Association's practice guideline for panic disorder is currently being revised). These are welcome updates to older guidelines published by New Zealand's National Health Committee (1998), as well as Expert Consensus Guidelines for treating OCD (March, Frances, Kahn, & Carpenter, 1997) and PTSD (Foa, Davidson, & Frances, 1999), developed by Expert Knowledge Systems.

Recommendations from across these guidelines are fairly consistent. They confirm that anxiety disorders are responsive to intervention, and that effective treatments include pharmacological approaches, psychological approaches (particularly cognitive and behavioral treatments), and combinations of these treatments. Part Five of this book provides a detailed review of these strategies for treating anxiety disorders. In this section, we provide a brief overview of effective treatments.

Biological Treatments

Comprehensive reviews of pharmacological treatments for anxiety disorders may be found in Swinson et al. 2006, as well as in Chapters 22, 24, 26, 28, and 30 of this volume. Effective medications exist for each of the anxiety disorders, with the exception of specific phobias, where the treatment of choice is almost always behavioral (in particular, exposure to feared situations and objects), though as-needed (p.r.n.) benzodiazepines may have a role for occasional use only. Generally, most first-line pharmacological treatments are antidepressants. For example, there is broad support for the use of selective serotonin reuptake inhibitors (SSRIs; e.g., citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline) for all of the anxiety disorders, except for specific phobia. Serotonin-norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine extended-release (and more recently, duloxetine) are also effective for many of the anxiety disorders. Newer antidepressants such as mirtazapine (a noradrenergic/specific serotonergic antidepressant or NaSSA) and reboxetine (a norepinephrine reuptake inhibitor) also show promise for treating several of the anxiety disorders, but much more research is needed. However, older antidepressants, such as tricyclic antidepressants and monoamine oxidase inhibitors (MAOIs), are used less frequently now than they were in the past because they tend to be more difficult to tolerate and are more dangerous in overdose.

Benzodiazepines (e.g., alprazolam, clonazepam, lorazepam, diazepam), typically introduced as a second-line treatment, primarily because of the risk of dependence, are still widely used—though oft-disparaged—in the treatment of anxiety disorders. There is now emerging evidence supporting the use of several anticonvulsants (e.g., gabapentin, pregabalin) for certain anxiety disorders, though further research is needed. Combining atypical antipsychotics (e.g., risperidone, olanzapine) with antidepressants may lead to improved outcomes for some patients with anxiety disorders such as OCD or PTSD. There is also evidence supporting the use of buspirone for GAD, and beta-adrenergic blockers (taken on a p.r.n. basis) may have a role in the treatment of discrete performance fears (e.g., fears of public speaking), though these medications are not supported for the treatment of generalized social anxiety disorder.

For treatment refractory cases of OCD, there is preliminary evidence from large case series supporting the use of specific neurosurgical procedures (e.g., cingulotomy, bilateral anterior capsulotomy) as a last option, though controlled studies are lacking (see Chapter 28). Finally, there is preliminary evidence supporting the use of several herbal products and other alternative treatments for particular anxiety disorders (see Chapter 34).

Psychological Treatments

Although there are a few preliminary studies supporting the use of client-centered psychotherapy, brief psychodynamic psychotherapy, and interpersonal psychotherapy for particular anxiety disorders (e.g., Lipsitz, Markowitz, Cherry, & Fyer, 1999; Milrod et al., 2007; Teusch, Böhme, & Gastpar, 1997), almost all research on psychological (p. 12) treatments for anxiety-based problems has focused on cognitive and behavioral approaches (for a review, see Swinson et al., 2006, as well as Chapters 23, 25, 27, 29, 31, 33, 35, 36, and 37 in this volume). Furthermore, some studies have found cognitive behavioral therapy (CBT) to be more effective for treating anxiety disorders than other approaches, such as supportive psychotherapy (e.g., Heimberg et al., 1990).

Cognitive behavioral therapy is not a single approach to treatment, but rather one that involves a wide variety of strategies that often differ across patients and across disorders. Although investigators have begun to study transdiagnostic approaches to treating anxiety disorders (see Chapter 33), most studies have tended to focus on the treatment of a single anxiety disorder. Evidence-based cognitive and behavioral strategies for anxiety disorders include psychoeducation (e.g., presenting a cognitive model of anxiety; discussing treatment options, etc.), in vivo exposure (i.e., exposure to feared situations and objects), exposure in imagination (e.g., to feared thoughts, images, and impulses), interoceptive exposure (i.e., exposure to feared physical sensations), prevention of compulsive rituals and other safety behaviors, cognitive restructuring (e.g., evaluating the evidence for anxiety-provoking beliefs), relaxation training, mindfulness and acceptance-based approaches, and skills training (e.g., social skills training, problem-solving training).

Variations on these approaches have also been studied. For example, applied tension is an effective treatment for blood and injection phobias. This treatment combines exposure (for reducing fear) with muscle tension exercises (for increasing blood pressure, thereby preventing fainting) (Öst, Fellenius, & Sterner, 1991). Exposure-based treatments have also been developed using virtual reality technology, and preliminary studies suggest that computer-generated, virtual reality exposures may be as effective as in vivo exposure for certain phobias (Emmelkamp, Bruynzeel, Drost, & van der Mast, 2001). Finally, eye movement desensitization and reprocessing (EMDR; a treatment that combines imaginal exposure with bilateral eye movements, as well as other strategies) has been studied for a number of anxiety disorders, though most of this work has been in the area of PTSD. Although research supports the effectiveness of EMDR for PTSD, there is no evidence that the eye movements add anything to the treatment, and critics have observed that the essential elements of EMDR are similar to those of other evidence-based psychological treatments, including exposure, for example (Lohr, Tolin, & Lilienfeld, 1998).

Table 1 lists well-supported psychological treatment strategies for each of the main anxiety disorders, as well as strategies for which support is preliminary, mixed, or tentative.

Combination Treatments

Large trials comparing medication, CBT, and their combination have been conducted for several anxiety disorders, including panic disorder (Barlow, Gorman, Shear, & Woods, 2000), social phobia (Davidson et al., 2004), and OCD (Foa et al., 2005). Preliminary evidence regarding combined treatments also exists for GAD (Bond, Wingrove, Curran, & Lader, 2002) and PTSD (Cohen, Mannarino, Perel, & Staron, 2007). Although a few studies have found combined treatments to be superior to either medication or CBT alone, most studies across the anxiety disorders have found combined treatments to be equivalent to monotherapies immediately following treatment (Black, 2006; Chapter 32, this volume). However, there is evidence that over the long term (once treatment has been discontinued), CBT alone leads to superior outcomes for the treatment of panic disorder, relative to those following medication alone or the combination of medication and CBT (Barlow et al., 2000). The long-term effects of treatment on other anxiety disorders remain to be studied. Also, most studies on combined treatment have studied the effects of beginning CBT and pharmacotherapy concurrently. Additional research on the sequential introduction of CBT and pharmacotherapy is needed.


Anxiety disorders include a diverse group of conditions that share a number of common features, such as a predominance of anxiety and fear, avoidance of feared situations and experiences, and reliance on safety behaviors designed to reduce perceived threat. There is strong evidence supporting the role of biological, psychological, and environmental factors in the cause and maintenance of anxiety disorders. Although anxiety disorders are often chronic conditions, most individuals experience a reduction in symptoms following treatment with medications, cognitive behavioral therapy, or a combination of these approaches. The remainder of this handbook provides detailed reviews on the phenomenology, etiology, assessment, and treatment of each of the main anxiety disorders, as well as for several related conditions. (p. 13)

Table 1. Summary of Psychological Treatment Strategies

Anxiety Disorder

Well-Established Strategiesa

Strategies with Preliminary Support or Mixed Support

Panic Disorder and Agoraphobia

● Psychoeducation

● Breathing retrainingb

● Cognitive restructuring

● Psychodynamic psychotherapyc

● Interoceptive exposure

● Experiential psychotherapyc

● In vivo exposure (for agoraphobia)

Social Anxiety Disorder

● Psychoeducation

● Applied relaxation trainingd

● Cognitive restructuring

● Virtual reality exposuree

● In vivo exposure

● Interpersonal Psychotherapye

● Simulated exposures (role plays)

● Social skills training

Specific Phobia

● In vivo exposure

● Applied tension (for blood and injection phobias ● Applied relaxationf

● Applied tension (for blood and injection phobias)

● Virtual reality exposureg

Generalized Anxiety Disorder

● Cognitive restructuring

● Mindfulness and acceptance-based strategiesh

● Progressive muscle relaxation

● Exposure to worry-related imageryi

● Problem-solving trainingi

● Prevention of worry behaviorsi

● Stimulus control strategies (e.g., scheduling times to worry)i

Obsessive-Compulsive Disorder

● Exposure and ritual prevention

● Exposure in imaginationj

● Cognitive restructuring

Posttraumatic Stress Disorder

● In vivo exposure

● Eye movement desensitization and reprocessing (EMDR)k

● Exposure in imagination

● Virtual reality exposurel

● Cognitive restructuring

● Progressive muscle relaxation

(a) Support for well-established treatment strategies can be found in Swinson et al., 2006, as well as in Chapter 23, 25, 27,29, 31, 33, 35, 36, and 37 in this volume.

(b) Although this strategy is often included in treatment protocols for panic disorder, there is little evidence that it adds to treatment outcome overall (Schmidt et al., 2000).

(c) Support is still very preliminary, based on a very small number of studies (e.g., Milrod et al., 2007; Teusch, Bohme, & Gastpar, 1997).

(d) Th is strategy involves combining relaxation training with exposure. Although preliminary studies suggest it is effective for reducing social anxiety (e.g., Ost, Jerremalm, & Johansson, 1981), there is no evidence that it is any more effective than exposure alone, and one study found that it is less effective than cognitive therapy (Clark et al., 2006).

(e) Success has been reported in a small number of trials using virtual reality for public speaking fears (Anderson, Zimand, Hodges, & Rothbaum, 2005; Klinger et al., 2005) and interpersonal psychotherapy (Lipsitz, Markowitz, Cherry, & Fyer, 1999).

(f) This strategy involves combining relaxation training with exposure. Although preliminary studies suggest it is effective for reducing phobic fear (e.g., in claustrophobia; öst, Johansson, & Jerremalm, 1982), there is no evidence that it is any more effective than exposure alone.

(g) A number of studies support the use of virtual reality for height phobias, flying phobias, and other specific phobias. A small number of studies have compared virtual exposure to live exposure, finding few differences (e.g., Emmelkamp, Bruynzeel, Drost, & van der Mast, 2001), though more comparative studies are needed.

(h) Success has been reported in a small number of uncontrolled trials (e.g., Roemer & Orsillo, 2007).

(i) These strategies have been included in a number of trials of CBT for GAD. However, dismantling studies are needed to determine whether they add any specific benefits beyond the other strategies included in standard treatments.

(g) This strategy has been included in a number of trials on the treatment of OCD. However, dismantling studies are needed to determine whether it adds any specific benefit beyond in vivo exposure and ritual prevention.

(k) Numerous studies support the use of EMDR for treating PTSD, though this treatment appears to be no more effective than other established treatments (Davidson & Parker, 2001). There is little evidence that the eye movements contribute to the effectiveness of EMDR, and outcomes are probably related to the effects of exposure and other treatment components (Davidson & Parker, 2001; Lohr, Tolin, & Lilienfeld, 1998).

(l) Support has been based primarily on small uncontrolled studies and case reports (e.g., Ready, Pollack, Rothbaum, & Alarcon, 2006; Rothbaum, Hodges, Ready, Graap, & Alarcon, 2001).


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