4.1.1 Clinical Description

Panic disorder consists of a series of recurrent, unexpected panic attacks coupled with the fear of future panic attacks. A panic attack is defined as a sudden or abrupt surge or fear or impending doom along with at least four physical or cognitive symptoms (listed below). The symptoms generally peak within a few minutes, although it seems much longer for the individual experiencing the panic attack.

There are two key components to panic disorder—the attacks are unexpected meaning there is nothing that triggers them, and they are recurrent meaning they occur multiple times. Because these panic attacks occur frequently and essentially “out of the blue,” they cause significant worry or anxiety in the individual as they are unsure of when the next attack will occur. In some individuals, significant behavioral changes such as fear of leaving their home or attending large events occur as the individual is fearful an attack will happen in one of these situations, causing embarrassment. Additionally, individuals report worry that other’s will think they are “going crazy” or losing control if they were to observe an individual experiencing a panic attack. Occasionally, an additional diagnosis of agoraphobia is given to an individual with panic disorder if their behaviors meet diagnostic criteria for this disorder as well (see more below).

The frequency and intensity of these panic attacks vary widely among individuals. Some people report panic attacks occurring once a week for months on end, others report more frequent attacks multiple times a day, but then experience weeks or months without any attacks. The intensity of symptoms also varies among individuals, with some individuals reporting experiencing nearly all 14 symptoms and others only reporting the minimum 4 required for the diagnosis. Furthermore, individuals report variability within their own panic attack symptoms, with some panic attacks presenting with more symptoms than others. It should be noted that at this time, there is no identifying information (i.e. demographic information) to suggest why some individuals experience panic attacks more frequently or more severe than others.

4.1.2 Epidemiology

Prevalence rates for panic disorder are estimated at around 2-3% in adults and adolescents. Higher rates of panic disorder are found in American Indians and non-Latino whites. Females are more commonly diagnosed than males with a 2:1 diagnosis rate—this gender discrepancy is seen throughout the lifespan. Although panic disorder can occur in young children, it is generally not observed in individuals younger than 14 years of age.

4.1.3 Comorbidity

Panic disorder rarely occurs in isolation, as many individuals also report symptoms of other anxiety disorders, major depression, and substance abuse. There is mixed evidence as to whether panic disorder precedes other comorbid psychological disorders—estimates suggest that 1/3 of individuals with panic disorder will experience depressive symptoms prior to panic symptoms whereas the remaining 2/3 will experience depressive symptoms concurrently or after the onset of panic disorder (APA, 2013).

Unlike some of the other anxiety disorders, there is a high comorbid diagnosis with general medical symptoms. More specifically, individuals with panic disorder are more likely to report somatic symptoms such as dizziness, cardiac arrhythmias, asthma, irritable bowel syndrome, and hyperthyroidism (APA, 2013). The relationship between panic symptoms and somatic symptoms is unclear; however, there does not appear to be a direct medical cause between the two.

4.1.4 Treatment

4.1.4.1 Cognitive Behavioral Therapy (CBT) 

CBT is the most effective treatment option for individuals with panic disorder as the focus is on correcting misinterpretations of bodily sensations (Craske & Barlow, 2014). Nearly 80 percent of people with panic disorder report complete remission of symptoms after mastering the following five components of CBT for panic disorder (Craske & Barlow, 2014).

1. Psychoeducation. Treatment begins by educating the client on the nature of panic disorder, the underlying causes of panic disorder, as well as the mechanisms that maintain the disorder such as the physical, cognitive, and behavioral response systems (Craske & Barlow, 2014). This part of treatment is fundamental in correcting any myths or misconceptions about panic symptoms, as they often contribute to the exacerbation of panic symptoms.
2. Self-monitoring. Self-monitoring, or the awareness of self-observation, is essential to the CBT treatment process for panic disorder. In this part of treatment, the individual is taught to identify the physiological cues immediately leading up to and during a panic attack.  The client is then encouraged to identify and document/record the thoughts and behaviors associated with these physiological symptoms. By bringing awareness to the symptoms, as well as the relationship between physical arousal and cognitive/behavioral responses, the client is learning the fundamental processes in which they can manage their panic symptoms (Craske & Barlow, 2014).
3. Relaxation training. Prior to engaging in exposure training, the individual must learn a relaxation technique to apply during the onset of panic attacks. While breathing training was once included as the relaxation training technique of choice for panic disorder, due to the high report of hyperventilation during panic attacks more recent research has failed to support this technique as effective in the use of panic disorder (Schmidt et al., 2000). Findings suggest that breathing retraining is more commonly misused as a means for avoiding physical symptoms as opposed to an effective physiological response to stress (Craske & Barlow, 2014). To replace the breathing retraining, Craske & Barlow (2014) suggest progressive muscle relaxation (PMR). In PMR, the client learns to tense and relax various large muscle groups throughout the body. Generally speaking, the client is encouraged to start at either the head or the feet, and gradually work their way up through the entire body, holding the tension for roughly 10 seconds before relaxing. The theory behind PMR is that in tensing the muscles for a prolonged period of time, the individual exhausts those muscles, forcing them (and eventually) the entire body to engage in relaxation (McCallie, Blum, & Hood, 2006).
4. Cognitive restructuring. Cognitive restructuring, or the ability to recognize cognitive errors and replace them with alternate, more appropriate thoughts, is likely the most powerful part of CBT treatment for panic disorder, aside from the exposure part. Cognitive restructuring involves identifying the role of thoughts in generating and maintaining emotions. The clinician encourages the individual to view these thoughts as “hypotheses” as opposed to facts, which allows the thoughts to be questioned and challenged. This is where the detailed recordings in the self-monitoring section of treatment are helpful. By discussing specifically what the client has recorded for the relationship between physiological arousal and thoughts/behaviors, the clinician is able to help the individual restructure the maladaptive thought processes to more positive thought processes which in return, helps to reduce fear and anxiety.
5. Exposure. Next, the client is encouraged to engage in a variety of exposure techniques such as in vivo exposure and interoceptive exposure, while also incorporating the cognitive restructuring and relaxation techniques previously learned in efforts to reduce and eliminate ongoing distress. Interoceptive exposure involves inducing panic specific symptoms to the individual repeatedly, for a prolonged time period, so that maladaptive thoughts about the sensations can be disconfirmed and conditional anxiety responses are extinguished (Craske & Barlow, 2014). Some examples of these exposure techniques are spinning a client repeatedly in a chair to induce dizziness and breathing in a paper bag to induce hyperventilation. These treatment approaches can be presented in a gradual manner; however, the client must endure the physiological sensations for at least 30 seconds to 1 minute to ensure adequate time for applying cognitive strategies to misappraisal of cognitive symptoms (Craske & Barlow, 2014). Interoceptive exposure is continued both in and outside of treatment until panic symptoms remit. Over time, the habituation of fear within an exposure session will ultimately lead to habituation across treatment, which leads to long-term remission of panic symptoms (Foa & McNally, 1996).  Occasionally, panic symptoms will return in individuals who report complete remission of panic disorder. Follow-up booster sessions reviewing the steps above is generally effective in eliminating symptoms again.

4.1.4.2 Pharmacological Interventions 

According to Craske & Barlow (2014), nearly half of people with panic disorder present to psychotherapy already on medication, likely prescribed by their primary care physician. Some researchers argue that anti-anxiety medications impede the progress of CBT treatment as the individual is not able to fully experience the physiological sensations during exposure sessions, thus limiting their ability to modify maladaptive thoughts maintaining the panic symptoms. Results from large clinical trials suggest no advantage during or immediately after treatment of combining CBT and medication (Craske & Barlow, 2014). Additionally, when medications were discontinued post-treatment, the CBT+ medication groups fared worse than the CBT treatment alone groups, thus supporting the theory that immersion in interoceptive exposure is limited by the use of medication. Therefore, it is suggested that medications are reserved for those who do not respond to CBT therapy alone (Kampman, Keijers, Hoogduin & Hendriks, 2002).

4.2.1 Clinical Description

Generalized anxiety disorder, commonly referred to as GAD, is a disorder characterized by an underlying excessive worry related to a wide range of events or activities. While many individuals experience some levels of worry throughout the day, individuals with GAD experience worry of a greater intensity and for longer periods of times than the average person. Additionally, they are often unable to control their worry through various coping strategies, which directly interferes with their ability to engage in daily social and occupational tasks. There are six characteristic symptoms of generalized anxiety disorder and in order to be diagnosed with the disorder, individuals must experience at least three of them. These symptoms are: feeling restless, being easily fatigued, having difficulty concentrating, feeling irritable, having muscle tension, experiencing problems with sleep.

4.2.2 Epidemiology

The prevalence rate for generalized anxiety disorder is estimated to be 3% of the general population, with nearly 6% of individuals experiencing GAD sometime during their lives. While it can present at any age, it generally appears first in childhood or adolescence. Similar to most anxiety-related disorders, females are twice as likely to be diagnosed with GAD as males (APA, 2013).

4.2.3 Comorbidity

There is a high comorbidity between generalized anxiety disorder and the other anxiety-related disorders, as well as major depressive disorder, suggesting they all share common vulnerabilities, both biological and psychological.

4.2.4 Treatment

4.2.4.1 Psychopharmacology

Benzodiazepines, a class of sedative-hypnotic drugs, originally replaced barbiturates as the leading anti-anxiety medication due to their less addictive nature, yet equally effective ability to calm individuals at low dosages. Unfortunately, as more research was conducted on benzodiazepines, serious side effects, as well as physical dependence have routinely been documented (NIMH, 2013). Due to these negative effects, selective serotonin-reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) are generally considered to be first-line medication options for those with GAD. Findings indicate a 30-50% positive response rate to these psychopharmacological interventions (Reinhold & Rickels, 2015). Unfortunately, none of these medications continue to provide any benefit once they are stopped; therefore, other more effective treatment options such as CBT, relaxation training, and biofeedback are often encouraged before the use of pharmacological interventions.

4.2.4.2 Rational-Emotive Therapy 

Rational emotive therapy was developed by Albert Ellis in the mid-1950s as one of the first forms of cognitive-behavioral therapy. Ellis proposed that individuals were not aware of the effect their negative thoughts had on their behaviors and various relationships and thus, identified a treatment aimed to address these thoughts in an effort to provide relief to those experiencing anxiety and depression. The goal of rational emotive therapy is to identify irrational, self-defeating assumptions, challenge the rationality of those assumptions, and to replace them with new more productive thoughts and feelings. It is proposed that through identifying and replacing these assumptions that one will experience relief of GAD symptoms (Ellis, 2014).

4.2.4.3 Cognitive Behavioral Therapy (CBT) 

CBT is among the most effective treatment options for a variety of anxiety disorders, including GAD. In fact, findings suggest 60% of individuals report a significant reduction/elimination in anxious thoughts one-year post-treatment (Hanrahan, Field, Jones, & Davy, 2013). The fundamental goal of CBT is a combination of cognitive and behavioral strategies aimed to identify and restructure maladaptive thoughts while also providing opportunities to utilize these more effective thought patterns through exposure based experiences. Through repetition, the individual will be able to identify and replace anxious thoughts outside of therapy sessions, ultimately reducing their overall anxiety levels (Borkovec, & Ruscio, 2001).

4.2.4.4 Biofeedback 

Biofeedback provides a visual representation of a clients’s physiological arousal. To achieve this feedback, a client is connected to a computer that provides continuous information on their physiological states. There are several ways a client can be connected to the computer. Among the most common is electromyography (EMG). EMG measures the amount of muscle activity currently experienced by the individual. An electrode is placed on a individuals’s skin just above a major muscle group- commonly the forearm or the forehead. Other common types of measurement are electroencephalography (EEG) which measures the neurofeedback or brain activity; heart rate variability (HRV) which measures autonomic activity such as heart rate or blood pressure; and galvanic skin response (GSR) which measures sweat.

Once the client is connected to the biofeedback machine, the clinician is able to walk the client through a series of relaxation scripts or techniques as the computer simultaneously measures the changes in muscle tension. The theory behind biofeedback is that in providing a client with a visual representation of changes in their physiological state, they become more skilled at voluntarily reducing their physiological arousal, and thus, their overall sense of anxiety or stress. While research has identified only a modest effect of biofeedback on anxiety levels, clients do report a positive experience with the treatment due to the visual feedback of their physiological arousal (Brambrink, 2004).

4.3.1 Clinical Description

Specific phobia is distinguished by an individual’s fear or anxiety specific to an object or a situation. While the amount of fear or anxiety related to the specific object or situation varies among individuals, it also varies related to the proximity of the object/situation. When individuals are face-to-face with their specific phobia, immediate fear is present. It should also be noted that these fears are more excessive and more persistent than a “normal” fear, often severely impacting one’s daily functioning (APA, 2013).

Individuals can experience multiple specific phobias at one time. In fact, nearly 75% of individuals with a specific phobia report fear in more than one object (APA, 2013).  When making a diagnosis of specific phobia, it is important to identify the specific phobic stimulus. Among the most commonly diagnosed specific phobias are animals, natural environments (height, storms, water), blood-injection-injury (needles, invasive medical procedures), or situational (airplanes, elevators, enclosed places; APA, 2013). Given the high percentage of individuals who experience more than one specific phobia, all specific phobias should be listed as a diagnosis in efforts to identify an appropriate treatment plan.

4.3.2 Epidemiology

The prevalence rate for specific phobias is 7-9% within the united states. While young children have a prevalence rate of approximately 5%, teens have nearly a double prevalence rate than that of the general public at 16%. There is a 2:1 ratio of females to males diagnosed with specific phobia; however, this rate changes depending on the different phobic stimuli. More specifically, animal, natural environment, and situational specific phobias are more commonly diagnosed in females, whereas blood-injection-injury phobia is reportedly diagnosed equally between genders.

4.3.3. Comorbidity

Seeing as the onset of specific phobias occurs at a younger age than most other anxiety disorders, it is generally the primary diagnosis with generalized anxiety disorder as an occasional comorbid diagnosis. It should be noted that children/teens diagnosed with a specific phobia are at an increased risk for additional psychopathology later in life. More specifically, other anxiety disorders, depressive disorders, substance-related disorders and somatic symptom disorders.

4.3.4 Treatment

4.3.4.1 Exposure Treatments 

While there are many treatment options for specific phobias, research routinely supports the behavioral techniques as the most effective treatment strategies. Seeing as the behavioral theory suggests phobias are developed via classical conditioning, the treatment approach revolves around breaking the maladaptive association developed between the object and fear. This is generally accomplished through exposure treatments. As the name implies, the individual is exposed to their feared stimuli. This can be done using several different approaches: systematic desensitization, flooding, and modeling. 

Systematic desensitization is an exposure technique that utilizes relaxation strategies to help calm the individual as they are presented with the fearful object. The notion behind this technique is that both fear and relaxation cannot exist at the same time; therefore, the individual is taught how to replace their fearful reaction with a calm, relaxing reaction. To begin, the client, with assistance from the clinician, will identify a fear hierarchy, or a list of feared objects/situations ordered from least fearful to most fearful. After learning intensive relaxation techniques, the clinician will present items from the fear hierarchy- starting from the least fearful object/subject- while the patient practices using the learned relaxation techniques. The presentation of the feared object/situation can be in person (in vivo exposure) or it can be imagined (imaginal exposure). Imaginal exposure tends to be less intensive than in vivo exposure; however, it is less effective than in vivo exposure in eliminating the phobia. Depending on the phobia, in vivo exposure may not be an option, such as with a fear of a tornado. Once the patient is able to effectively employ relaxation techniques to reduce their fear/anxiety to a manageable level, the clinician will slowly move up the fear hierarchy until the individual does not experience excessive fear of any objects on the list.

Another exposure technique is flooding. In flooding, the clinician does not utilize a fear hierarchy, but rather repeatedly exposes the individual to their most feared object/subject. Similar to systematic desensitization, flooding can be done in either in vivo or imaginal exposure. Clearly, this technique is more intensive than the systematic or gradual exposure to feared objects. Because of this, patients are at a greater likelihood of dropping out of treatment, thus not successfully overcoming their phobias.

Finally, modeling is a common technique that is used to treat specific phobias (Kelly, Barker, Field, Wilson, & Reynolds, 2010). In this technique, the clinician approaches the feared object/subject while the patient observes. Like the name implies, the clinician models appropriate behaviors when exposed to the feared stimulus, implying that the phobia is irrational. After modeling several times, the clinician encourages the patient to confront the feared stimulus with the clinician, and then ultimately, without the clinician.

Section Learning Objectives

• Describe how social anxiety disorder presents itself.
• Describe the epidemiology of social anxiety disorder.
• Indicate which disorders are commonly comorbid with social anxiety disorder.
• Describe the treatment options for social anxiety disorder.

4.4.1 Clinical Description

For social anxiety disorder (formerly known as social phobia), the anxiety is directed toward the fear of social situations, particularly those in which an individual can be evaluated by others. More specifically, the individual is worried that they will be judged negatively and viewed as stupid, anxious, crazy, boring, unlikeable, or boring to name a few. Some individuals report feeling concerned that their anxiety symptoms will be obvious to others via blushing, stuttering, sweating, trembling, etc. These fears severely limit an individual’s behavior in social settings. For example, an individual may avoid holding drinks or plates if they know they will tremble in fear of dropping or spilling food/water. Additionally, if one is known to sweat a lot in social situations, they may limit physical contact with others, refusing to shake hands.

Unfortunately, for those with social anxiety disorder, all or nearly all social situations provoke this intense fear. Some individuals even report significant anticipatory fear days or weeks before a social event is to occur. This anticipatory fear often leads to avoidance of social events in some individuals; others will attend social events with a marked fear of possible threats. Because of these fears, there is a significant impact on one’s social and occupational functioning.

It is important to note that the cognitive interpretation of these social events is often excessive and out of proportion to the actual risk of being negatively evaluated. There are instances where one may experience anxiety toward a real threat such as bullying or ostracizing. In this instance, social anxiety disorder would not be diagnosed as the negative evaluation and threat are real.

4.4.2 Epidemiology

The overall prevalence rate of social anxiety disorder is significantly higher in the United States than in other countries worldwide, with an estimated 7% of the US population diagnosed with social anxiety disorder. Within the US, the prevalence rate remains the same among children through adults; however, there appears to a significant decrease in the diagnosis of social anxiety disorder among older individuals. With regards to gender, there is a higher diagnosis rate in females than males. This gender discrepancy appears to be larger in children/adolescents than adults.

4.4.3 Comorbidity

Among the most common comorbid diagnoses with social anxiety disorder are other anxiety-related disorders, major depressive disorder, and substance-related disorders. Generally speaking, social anxiety disorders will precede that of other mental health disorders, with the exception of separation anxiety disorder and specific phobia, seeing as these two disorders are more commonly diagnosed in childhood (APA, 2013). The high comorbidity rate among anxiety-related disorders and substance-related disorders is likely related to the efforts of self-medicating. For example, an individual with social anxiety disorder may consume larger amounts of alcohol in social settings in efforts to alleviate the anxiety of the social situation.

4.4.4 Treatment

4.4.4.1 Exposure 

A hallmark treatment approach for all anxiety disorders is exposure. Specific to social anxiety disorder, the individual is encouraged to engage in social situations where they are likely to experience increased anxiety. Initially, the clinician will engage in role-playing of various social situations with the client so that he/she can practice social interactions in a safe, controlled environment (Rodebaugh, Holaway, & Heimberg, 2004). As the client becomes habituated to the interaction with the clinician, the clinician and client may venture outside of the treatment room and engage in social settings with random strangers at various locations such as fast food restaurants, local stores, libraries, etc. The client is encouraged to continue with these exposure based social interactions outside of treatment to help reduce anxiety related to social situations.

4.4.4.2 Social Skills Training 

This treatment is specific to social anxiety disorder as it focuses on skill deficits or inadequate social interactions displayed by the client that contributes to the negative social experiences and anxiety. The clinician may use a combination of skills such as modeling, corrective feedback, and positive reinforcement to provide feedback and encouragement to the client regarding his/her behavioral interactions (Rodebaugh, Holaway, & Heimberg, 2004). By incorporating the clinician’s feedback into their social repertoire, the client can engage in positive social behaviors outside of the treatment room in hopes to improve overall social interactions and reduce ongoing social anxiety.

4.4.4.3 Cognitive Restructuring 

While exposure and social skills training are helpful treatment options, research routinely supports the need to incorporate cognitive restructuring as an additive component in treatment to provide substantial symptom reduction. Here the client will work with the therapist to identify negative, automatic thoughts that contribute to the distress in social situations. The clinician can then help the client establish new, positive thoughts to replace these negative thoughts. Research indicates that implementing cognitive restructuring techniques before, during, and after exposure sessions enhances the overall effects of treatment of social anxiety disorder (Heimberg & Becker, 2002).

Section Learning Objectives

• Describe how agoraphobia presents itself.
• Describe the epidemiology of agoraphobia.
• Indicate which disorders are commonly comorbid with agoraphobia.
• Describe the treatment options for agoraphobia.

4.5.1 Clinical Description

Similar to GAD, agoraphobia is defined as an intense fear triggered by a wide range of situations; however, unlike GAD, agoraphobia’s fears are related to situations in which the individual is in public situations where escape may be difficult. In order to receive a diagnosis of agoraphobia, there must be a presence of fear in at least two of the following situations: using public transportation such as planes, trains, ships, buses; being in large, open spaces such as parking lots or on bridges; being in enclosed spaces like stores or movie theaters; being in a large crowd similar to those at a concert; or being outside of the home in general (APA, 2013). When an individual is in one (or more) of these situations, they experience significant fear, often reporting panic-like symptoms (see Panic Disorder). It should be noted that fear and anxiety related symptoms are present every time the individual is presented with these situations. Should symptoms only occur occasionally, a diagnosis of agoraphobia is not warranted.

Due to the intense fear and somatic symptoms, individuals will go to great lengths to avoid these situations, often preferring to remain within their home where they feel safe, thus causing significant impairment in one’s daily functioning. They may also engage in active avoidance, where the individual will intentionally avoid agoraphobic situations. These avoidance behaviors may be behavioral, including having food delivery to avoid going to grocery store or only taking a job that does not require the use of public transportation, or cognitive, by using distraction and various other cognitive techniques to successfully get through the agoraphobic situation.

4.5.2 Epidemiology

The yearly prevalence rate for agoraphobia across the lifespan is roughly 1.7%. Females are twice as likely as males to be diagnosed with agoraphobia (notice the trend…). While it can occur in childhood, agoraphobia typically does not develop until late adolescence/early adulthood and typically tapers off in later adulthood.

4.5.3 Comorbidity

Similar to the other anxiety disorders, comorbid diagnoses include other anxiety disorders, depressive disorders, and substance use disorders, all of which typically occur after the onset of agoraphobia (APA, 2013). Additionally, there is also a high comorbidity between agoraphobia and PTSD. While agoraphobia can be a symptom of PTSD, an additional diagnosis of agoraphobia is made when all symptoms of agoraphobia are met in addition to the PTSD symptoms.

4.5.4 Treatment

Similar to the treatment approaches for specific phobias, exposure-based treatment techniques are among the most effective treatment options for individuals with agoraphobia; however, unlike the high success rate in specific phobias, exposure-based treatment for agoraphobia has been less effective in providing complete relief of the disorder. The success rate may be impacted by the high comorbidity rate of agoraphobia and panic disorder. Because of the additional presentation of panic symptoms, exposure-based treatments alone are not the most effective in eliminating symptoms as residual panic symptoms often remain (Craske & Barlow, 2014). Therefore, the best treatment approach for those with agoraphobia and panic disorder is a combination of exposure and CBT techniques (see panic disorder treatment).

For individuals with agoraphobia without panic symptoms, the use of group therapy in combination with individual exposure-based therapy has been identified as a successful treatment option. The group therapy format allows the individual to engage in exposure-based field trips to various community locations, while also maintaining a sense of support and security from a group of individuals whom they know. Research indicates that this exposure based type of treatment provides improvement for nearly 60% to 80% of patients with agoraphobia; however, there is a relatively high rate of partial relapse suggesting that long-term treatment or booster sessions at a minimum should be continued for several years (Craske & Barlow, 2014).

4.6.1 Biological

4.6.1.1 Genetic Influences

While genetics have been known to contribute to the presentation of anxiety symptoms, the interaction between genetics and stressful environmental influences accounts for more of anxiety disorders than genetics alone (Bienvenu, Davydow, & Kendler, 2011). The quest to identify specific genes that may predispose individuals to develop anxiety disorders has lead researchers to the serotonin transporter gene (5-HTTLPR). Mutation of the 5-HTTLPR gene has been found to be related to a reduction in serotonin activity and an increase in anxiety-related personality traits (Munafo, Brown, & Hairiri, 2008).

4.6.1.2 Neurobiological Structures

Researchers have identified several brain structures and pathways that are likely responsible for anxiety responses. Among those structures is the amygdala, the area of the brain that is responsible for storing memories related to emotional events (Gorman, Kent, Sullivan, & Coplan, 2000). When presented with a fearful situation, the amygdala initiates a reaction in efforts to prepare the body for a response. First, the amygdala triggers the hypothalamic-pituitary-adrenal (HPA) axis to prepare for immediate action— either to fight or flight. The second pathway is activated by the feared stimulus itself, by sending a sensory signal to the hippocampus and prefrontal cortex, to determine if the threat is real or imagined. If it is determined that no threat is present, the amygdala sends a calming response to the HPA axis, thus reducing the level of fear. If there is a threat present, the amygdala is activated, producing a fear response.

Specific to panic disorder is the implication of the locus coeruleus, the brain structure that serves as an “on-off” switch for norepinephrine neurotransmitters. It is believed that increased activation of the locus coeruleus results in panic like symptoms; therefore, individuals with panic disorder may have a hyperactive locus coeruleus, leaving them more susceptible to experience more intense and frequent physiological arousal than the general public (Gorman, Kent, Sullivan, & Coplan, 2000). This theory is supported by studies in which individuals experienced increased panic symptoms following injection of norepinephrine (Bourin, Malinge, & Guitton, 1995). Unfortunately, norepinephrine and the locus coeruleus fail to fully explain the development of panic disorder, as treatment would be much easier if only norepinephrine was implicated. Therefore, researchers argue that a more complex neuropathway is likely implicated in the development of panic disorder. More specifically, the corticostriatal-thalamocortical (CSTC) circuit, also known as the fear-specific circuit, is theorized as a major contributor to panic symptoms (Gutman, Gorman, & Hirsch, 2004). When an individual is presented with a frightening object or situation, the amygdala is activated, sending a fear response to the anterior cingulate cortex and the orbitofrontal cortex. Additional projection from the amygdala to the hypothalamus activates endocrinologic responses to fear- releasing adrenaline and cortisol to help prepare the body to fight or flight (Gutman, Gorman, & Hirsch, 2004). This complex pathway supports the theory that panic disorder is mediated by several neuroanatomical structures and their associated neurotransmitters.

4.6.2 Psychological

4.6.2.1 Cognitive 

The cognitive perspective on the development of anxiety disorders centers around dysfunctional thought patterns. Maladaptive assumptions are routinely observed in individuals with anxiety disorders, as they often interpret events as dangerous and overreact to potentially stressful events, which contributes to a heightened overall anxiety level. These negative appraisals, in combination with a biological predisposition to anxiety likely contribute to the development of anxiety symptoms (Gallagher et al., 2013).

Sensitivity to physiological arousal not only contributes to anxiety disorders in general, but also for panic disorder where individuals experience various physiological sensations and misinterpret them as catastrophic. One explanation for this theory is that individuals with panic disorder are actually more susceptible to more frequent and intensive physiological symptoms than the general public (Nillni, Rohan, & Zvolensky, 2012). Others argue that these individuals have had more trauma-related experiences in the past, and therefore, are quick to misevaluate their physical symptoms as a potential threat. This misevaluation of symptoms as impending disaster likely maintain symptoms as the cognitive misinterpretations to physiological arousal creates a negative feedback loop, leading to more physiological changes.

Social anxiety is also largely explained by cognitive theorists. Individuals with social anxiety disorder tend to hold unattainable or extremely high social beliefs and expectations. Furthermore, they often engage in preconceived maladaptive assumptions that they will behave incompetently in social situations and that their behaviors will lead to terrible consequences. Because of these beliefs, they anticipate social disasters will occur and therefore, avoid social encounters (or limit them to close friends/family members) in efforts to prevent the disaster (Moscovitch et al., 2013). Unfortunately, these cognitive appraisals are not only isolated before and during the event. Individuals with social anxiety disorder will also evaluate the social event after it has taken place, often obsessively reviewing the details (i.e., ruminating over social events). This over-evaluation of social performance negatively reinforces future avoidance of social situations.

4.6.2.2 Behavioral 

The behavioral explanation for the development of anxiety disorders is largely reserved for phobias- both specific and social phobia. More specifically, behavioral theorists focus on classical conditioning – when two events that occur close together become strongly associated with one another, despite their lack of causal relationship. Watson and Rayner’s (1920) infamous Little Albert experiment is an example of how classical conditioning can be used to induce fear through associations. In this study, Little Albert developed a fear of white rats by pairing a white rate with a loud sound. This experiment, although lacking ethical standards, was groundbreaking in the development of learned behaviors. Over time, researchers have been able to replicate these findings (in more ethically sound ways) to provide further evidence of the role of classical conditioning in the development of phobias.

4.6.2.3 Modeling

Modeling is another behavioral explanation of the development of specific and social phobias. In modeling, an individual acquires a far through observation and imitation (Bandura & Rosenthal, 1966). For example, when a young child observes their parent display irrational fears of an animal, the child may then begin to display similar behaviors. Similarly, observing another individual being ridiculed in a social setting may increase the chances of the development of social anxiety, as the individual may become fearful that they would experience a similar situation in the future. It is speculated that the maintenance of these phobias is due to the avoidance of the feared item or social setting, thus preventing the individual from learning that the item/social situation is not something that should be feared.

While modeling and classical conditioning largely explain the development of phobias, there is some speculation that the accumulation of a large number of these learned fears will develop into GAD. Through stimulus generalization, or the tendency for the conditioned stimulus to evoke similar responses to other conditions, a fear of one item (such as the dog) may become generalized to other items (such as all animals). As these fears begin to grow, a more generalized anxiety may present, as opposed to a specific phobia.

 4.6.3. Sociocultural

Finally, we will review the social constructs that contribute to and maintain anxiety disorders. While characteristics such as living in poverty, experiencing significant daily stressors, and increased exposure to traumatic events are all identified as major contributors to anxiety disorders, additional sociocultural influences such as gender and discrimination have also received a great deal of attention.

Gender has largely been researched within anxiety disorders due to the consistent discrepancy in diagnosis rate between men and women. As previously discussed, women are routinely diagnosed with anxiety disorders more often than men, a trend that is observed throughout the entire lifespan. One potential explanation for this discrepancy is the influence of social pressures on women. Women are more susceptible to experience traumatic experiences throughout their life, which may contribute to anxious appraisals of future events. Furthermore, women are more likely to use emotion-focused coping, which is less effective in reducing distress than problem-focused coping (McLean & Anderson, 2009). These factors may increase levels of stress hormones (e.g., cortisol) within women that leave them susceptible to develop symptoms of anxiety. Therefore, it appears a combination of genetic, environmental, and social factors may explain why women tend to be diagnosed with anxiety disorders more often than men.

Exposure to discrimination and prejudice, particularly relevant to ethnic minority and other marginalized groups, can also impact an individual’s anxiety level. Discrimination and prejudice contribute to negative interactions, which is directly related to negative affect and an overall decline in mental health (Gibbons et al., 2014). The repeated exposure to discrimination and prejudice over time can lead to fear responses in individuals, along with subsequent avoidance of social situations in efforts to protect themselves emotionally.

Anxiety Recap

The discussion included Generalized Anxiety Disorder, Specific Phobias, Agoraphobia, Social Anxiety Disorder, and Panic Disorder. As with other chapters in this book, we discussed the clinical presentation, epidemiology, comorbidity, and treatment of the anxiety disorders. Etiology was also discussed in the context of biological, psychological, and sociocultural theories.

Obsessive-Compulsive and Related Disorders

Chapter Learning Outcomes

• Describe obsessive-compulsive disorder and body dysmorphic disorder.
• Describe the epidemiology of obsessive-compulsive disorder.
• Describe comorbidities of obsessive-compulsive disorder and body dysmorphic disorder.
• Describe the etiology of these disorders.
• Describe treatment options for these disorders.

Clinical Description

Obsessive-compulsive disorder, more commonly known as OCD, requires the presence of obsessions and/or compulsions. Obsessions are defined as repetitive and intrusive thoughts, urges, or images. These obsessions are persistent, time-consuming, and unwanted, often causing significant distress and impairment in an individual’s daily functioning. Common obsessions are contamination (dirt on self or objects), errors of uncertainty regarding daily behaviors (locking a door, turning off appliances), thoughts of physical harm or violence, and orderliness, to name a few (Cisler, Adams, et. al., 2011; Yadin & Foa, 2009). Often the individual will try to ignore these thoughts, urges, or images. When they are unable to ignore them, the individual will engage in compulsatory behaviors to alleviate the anxiety.

Compulsions are defined as repetitive behaviors or mental acts that an individual typically performs in response to an obsession. Common examples of compulsions are checking (i.e. repeatedly checking if the stove is turned off even though the first four times they checked it was off), counting (i.e. flicking the lights off and on 5 times), hand washing, organizing objects in a symmetrical manner, and repeating specific words. These compulsive behaviors are typically performed in an attempt to alleviate the anxiety associated with the obsessive thoughts. For example, an individual may feel as though his hands are dirty after using utensils at a restaurant. He may obsess over this thought for a period of time, impacting his ability to interact with others or complete a specific task. This obsession will ultimately lead to the individual performing a compulsion where he will wash his hands with extremely hot water to rid all the germs, or even wash his hands a specified number of times if he also has a counting compulsion. At this point, the individual’s anxiety may be temporarily relieved.

These obsessions and compulsions are more excessive than the typical “cleanliness” as they consume a large part of the individual’s day. Indeed, in order to be considered clinical OCD, the obsessions or compulsions must consume more than 1 hour per day, cause distress, or result in impairment in functioning. Given the example above, an individual with a fear of contamination may refuse to eat out at restaurants or may bring his own utensils with him and insist on using them when he is not eating at home.

Epidemiology

The one-year prevalence rate for OCD is approximately 1.2% both in the US, and worldwide (APA, 2013). OCD has a balanced sex ratio in adults; however, in childhood, boys are diagnosed more frequently than girls (APA, 2013). With respect to gender and symptoms, females are more likely to be diagnosed with cleaning-related obsessions and compulsions, whereas males are more likely to display symptoms related to forbidden thoughts and symmetry (APA, 2013). Additionally, males have an earlier age of onset (5-15 yrs) compared to women (20-24 yrs; Rasmussen & Eisen, 1990). Approximately two-thirds of all individuals with OCD had some symptoms present before the age of 15 (Rasmussen & Eisen, 1990). Overall the average age of onset of OCD iis 19.5 years.

Comorbidity

There is a high comorbidity rate between OCD and other anxiety disorders. Nearly 76% of individuals with OCD will be diagnosed with another anxiety disorder, most commonly panic disorder, social anxiety disorder, generalized anxiety disorder, or a specific phobia (APA, 2013). Additionally, 63% of those with OCD will also be diagnosed with a mood disorder (APA, 2013).

There is a high comorbidity rate between OCD and tic disorder, particularly in males with an onset of OCD in childhood. Children presenting with early-onset OCD typically have a different presentation of symptoms than traditional OCD. Research has also indicated a strong triad of OCD, Tic disorder, and attention-deficit/hyperactivity disorder in children. Due to this triad of psychological disorders, it is believed there is a neurobiological mechanism at fault for the development and maintenance of the disorders.

It should be noted that there are several disorders- schizophrenia, bipolar disorder, eating disorders, and Tourettes – where there is a higher incidence of OCD than the general public (APA, 2013). Therefore, clinicians who have a client diagnosed with one of the disorders above, should also routinely assess him/her for OCD.

Etiology

Biological

There are a few biological explanations for obsessive-compulsive related disorders including: hereditary transmission, neurotransmitter deficits, and abnormal functioning in brain structures.

Hereditary Transmission

With regards to heritability studies, twin studies routinely support the role of genetics in the development of obsessive-compulsive behaviors, as monozygotic twins have a substantially greater concordance rate (80-87%) than dizygotic twins (47-50%; Carey & Gottesman, 1981; van Grootheest, Cath, Beekman, & Boomsma, 2005). Additionally, first degree relatives of individuals diagnosed with OCD are twice as likely to develop OCD (APA, 2013).

Interestingly, a study conducted by Nestadt and colleagues (2000) exploring the familial role in the development of obsessive-compulsive disorder found that family members of individuals with OCD had higher rates of both obsessions and compulsions than control families; however, obsessions were more specific to the family members than that of the disorder. This suggests that there is a stronger heritability association for obsessions than compulsions. This study also found a relationship between age of onset of OCD symptoms and family heritability. Individuals who experienced an earlier age of onset, particularly before age 17, were found to have more first-degree relatives diagnosed with OCD. In fact, after the age of 17, there was no relationship between family diagnoses, suggesting those who develop OCD at an older age may have a different diagnostic origin (Nestadt, et al., 2000).

Neurotransmitters

Neurotransmitters, particularly serotonin have been identified as a contributing factor to obsessive and compulsive behaviors. This discovery was actually on accident. When individuals with depression and comorbid OCD were given antidepressant medications clomipramine and/or fluoxetine (both of which increase levels of serotonin) to mediate symptoms of depression, not only did they report a significant reduction in their depressive symptoms, but they also experienced significant improvement in their symptoms of OCD (Bokor & Anderson, 2014). Interestingly enough, antidepressant medications that do not affect serotonin levels are not effective in managing obsessive and compulsive symptoms, thus offering additional support for deficits of serotonin levels as an explanation of obsessive and compulsive behaviors (Sinopoli, Burton, Kronenberg, & Arnold, 2017; Bokor & Anderson, 2014). More recently, there has been some research implicating the involvement of additional neurotransmitters – glutamate, GABA, and dopamine – in the development and maintenance of OCD, although future studies are still needed to draw definitive conclusions (Marinova, Chuang, & Fineberg, 2017).

Brain Structures

Seeing as neurotransmitters have a direct involvement in the development of obsessive-compulsive behaviors, it’s only logical that brain structures that house these neurotransmitters also likely play a role in symptom development. Neuroimaging studies implicate the brain structures and circuits in the frontal lobe, more specifically, the orbitofrontal cortex, which is located just above each eye (Marsh et al., 2014). This brain region is responsible for mediating strong emotional responses and converts them into behavioral responses. Once the orbitofrontal cortex receives sensory/emotional information via sensory inputs, it transmits this information through impulses. These impulses are then passed on to the caudate nuclei which filter through the many impulses received, passing along only the strongest impulses to the thalamus. Once the impulses reach the thalamus, the individual essentially reassesses the emotional response and decides whether or not to act behaviorally (Beucke et al., 2013). It is believed that individuals with obsessive-compulsive behaviors experience overactivity of the orbitofrontal cortex and a lack of filtering in the caudate nuclei, thus causing too many impulses to be transferred to the thalamus (Endrass et al., 2011). Further support for this theory has been shown when individuals with OCD experience brain damage to the orbitofrontal cortex or caudate nuclei and experience remission of OCD symptoms (Hofer et al., 2013).

 Cognitive

Cognitive theorists believe that OCD behaviors occur due to an individual’s distorted thinking and negative cognitive biases. More specifically, individuals with OCD are more likely to overestimate the probability of threat and harm, to have an inflated sense of responsibility for preventing harm, to think thoughts are important and need to be controlled, and to be perfectionistic. Additionally, some research has indicated that those with OCD also experience disconfirmatory bias, which causes the individual to seek out evidence that proves they failed to perform the ritual or compensatory behavior incorrectly (Sue, Sue, Sue, & Sue, 2017). Finally, individuals with OCD often report the inability to trust themselves and their instincts, and therefore, feel the need to repeat the compulsive behavior multiple times to ensure it is done correctly. These cognitive biases are supported throughout research studies that repeatedly find that individuals with OCD experience more intrusive thoughts than those without OCD (Jacob, Larson, & Storch, 2014).

Now that we have identified that individuals with OCD experience cognitive biases and that these biases contribute to the obsessive and compulsive behaviors, we have yet to identify why these cognitive biases occur. Everyone has times when they have repetitive or intrusive thoughts such as: “Did I turn the oven off after cooking dinner?” or “Did I remember to lock the door before I left home?” Fortunately, most individuals are able to either check once or even forgo checking after they confidently talk themselves through their actions, ensuring that the behavior in question was or was not completed. Unfortunately, individuals with OCD are unable to neutralize these thoughts without performing a ritual as a way to put themselves at ease. As you will see in more detail in the behavioral section below, the behaviors (compulsions) used to neutralize the thoughts (obsessions) provide a temporary relief to the individual. As the individual is continually exposed to the obsession and repeatedly engages in the compulsive behaviors to neutralize the anxiety, the behavior is repeatedly reinforced, thus becoming a compulsion. This theory is supported by studies where individuals with OCD report using more neutralizing strategies and report significant reductions in anxiety after employing these neutralizing techniques (Jacob, Larson, & Storch, 2014; Salkovskis, et al., 2003).

Behavioral

The behavioral explanation of obsessive-compulsive disorder focuses on the explanation of compulsions rather than obsessions. Behaviorists believe that these compulsions begin with and are maintained by the classical conditioning. As you may remember, classical conditioning occurs when an unconditioned stimulus is paired with a conditioned stimulus to produce a conditioned response. How does this help explain OCD? Well, an individual with OCD may experience negative thoughts or anxieties related to an unpleasant event (obsession; unconditioned stimulus). These thoughts/anxieties cause significant distress to the individual, and therefore, they seek out some kind of behavior (compulsion) to alleviate these threats (conditioned stimulus). This provides temporary relief to the individual, thus reinforcing the compulsive behaviors used to alleviate the threat. Over time, the conditioned stimulus (compulsive behaviors) are reinforced due to the repeated exposure of the obsession and the temporary relief that comes with engaging in these compulsive behaviors.

Strong support for this theory is the fact that the behavioral treatment option for OCD – exposure and response prevention – is among the most effective treatments for these disorders. As you will read below, this treatment essentially breaks the classical conditioning associated with the obsessions and compulsions through extinction (by preventing the individual from engaging in the compulsive behavior until anxiety is reduced).

Treatment

Exposure and Response Prevention 

Treatment of OCD has come a long way in recent years. Among the most effective treatment options is exposure and response prevention (March, Frances, Kahn, & Carpenter, 1997). First developed by psychiatrist Victor Meyer (1966), individuals are repeatedly exposed to their obsession, thus causing anxiety/fears, while simultaneously being prevented from engaging in their compulsive behaviors. Exposure sessions are often done in vivo, or in real life, via videos, or even imaginary, depending on the type of obsession.

Prior to beginning the exposure and response prevention exercises, the clinician must teach the client relaxation techniques for them to engage to cope with the distress of being exposed to the obsession. Once relaxation techniques are taught, the clinician and client will develop a hierarchy of obsessions. Treatment will start at those with the lowest amount of distress to ensure the client has success with treatment and to reduce the likelihood the client will withdrawal from treatment.

Within the hierarchy of obsessions, the individual is gradually exposed to their obsession. For example, an individual obsessed with germs might first watch a person sneeze on the computer in session. Once anxiety is managed and compulsions are resisted at this level of exposure, the individual would move on to being present in the same room as a sick individual, to eventually shaking hands with someone obviously sick, each time helping the client resist the compulsion to engage in the compulsive behavior. Once this level of the hierarchy is managed, they would move on to the next obsession and so forth until the entire list is complete.

Exposure and response prevention is very effective in treating individuals with OCD. In fact, some studies suggest up to an 86% response rate when treatment is completed (Foa et al., 2005). The largest barrier to treatment with OCD is getting clients to commit to treatment, as the repeated exposures and prevention of compulsive behaviors can be quite distressing to clients.

Psychopharmacology

There has been minimal support for the treatment of OCD with medication alone. This is likely due to the temporary resolution of symptoms during medication use. Among the most effective medications are those that inhibit the reuptake of serotonin (e.g., clomipramine or SSRI’s). Reportedly, up to 60% of people do show improvement in symptoms while taking these medications; however, symptoms are quick to return when medications are discontinued (Dougherty, Rauch, & Jenike, 2002). While there has been some promise in a combined treatment option of exposure and response prevention and SSRIs, these findings were not superior to exposure and response prevention alone, suggesting that the inclusion of medication in treatment does not provide any added benefit (Foa et al., 2005).

Clinical Description

Body Dysmorphic Disorder (BDD) is another obsessive-compulsive disorder, however, the focus of these obsessions are with a perceived defect or flaw in physical appearance. A key feature of these obsessions with defects or flaws are that they are not observable to others. An individual who has a congenital facial defect or a burn victim who is concerned about scars are not examples of an individual with BDD. The obsessions related to one’s appearance can run the spectrum from feeling “unattractive” to “looking hideous.” While any part of the body can be a concern for an individual with BDD, the most commonly reported areas are skin (e.g., acne, wrinkles, skin color), hair (e.g., thinning hair or excessive body hair), or nose (e.g., size, shape).

The distressing nature of the obsessions regarding one’s body, often drive individuals with BDD to engage in compulsive behaviors that take up a considerable amount of time. For example, an individual may repeatedly compare her body to other people’s bodies in the general public; repeatedly look at herself in the mirror; engage in excessive grooming which includes using make-up to modify her appearance. Some individuals with BDD will go as far as having numerous plastic surgeries in attempts to obtain the “perfect” appearance. The problem is plastic surgery does not usually resolve the issue after all the physical defect or flaw is not observable to others. While most of us are guilty of engaging in some of these behaviors, to meet criteria for BDD, one must spend a considerable amount of time preoccupied with his/her appearance (i.e., on average 3-8 hours a day), as well as display significant impairment in social, occupational, or other areas of functioning.

Epidemiology

The point prevalence rate for BDD among U.S. adults is 2.4% (APA, 2013). Internationally, this rate drops to 1.7% –1.8% (APA, 2013). Despite the difference between the national and international prevalence rates, the symptoms across races and cultures are similar.

Gender-based prevalence rates indicate a fairly balanced sex ratio (2.5% females; 2.2% males; APA, 2013). While the diagnosis rates may be different, general symptoms of BDD appear to be the same across genders with one exception: males tend to report genital preoccupations, while females are more likely to present with a comorbid eating disorder.

Comorbidity

While research on BDD is still in its infancy, initial studies suggest that major depressive disorder is the most common comorbid psychological disorder (APA, 2013). Major depressive disorder typically occurs after the onset of BDD. Additionally, there are some reports of social anxiety, OCD, and substance-related disorders (likely related to muscle enhancement; APA, 2013).

Etiology

Initial studies exploring genetic factors for BDD indicate a hereditary influence as the prevalence of BDD is elevated in first degree relatives of people with BDD. Interestingly, the prevalence of BDD is also heightened in first degree relatives of individuals with OCD (suggesting a shared genetic influence to these disorders).

However, environmental factors appear to play a larger role in the development of BDD than OCD (Ahmed, et al., 2014; Lervolino et al., 2009). Specifically, it is believed that negative life experiences such as teasing in childhood, negative social evaluations about one’s body, and even childhood neglect and abuse may contribute to BDD. Cognitive research has further discovered that people with BDD tend to have an attentional bias towards beauty and attractiveness, selectively attending to words related to beauty and attractiveness. Cognitive theories have also proposed that individuals with BDD have dysfunctional beliefs that their worth is inherently tied to their attractiveness and hold attractiveness as one of their primary core values. These beliefs are further reinforced by our society, which overly values and emphasizes beauty.

Treatment

Seeing as though there are strong similarities between OCD and BDD, it should not come as a surprise that the only two effective treatments for BDD are those that are effective in OCD. Exposure and response prevention has been successful in treating symptoms of BDD, as clients are repeatedly exposed to their body imperfections/obsessions and prevented from engaging in compulsions used to reduce their anxiety (Veale, Gournay, et al., 1996; Wilhelm, Otto, Lohr, & Deckersbach, 1999).

The other treatment option, psychopharmacology, has also been shown to reduce symptoms in individuals diagnosed with BDD. Similar to OCD, medications such as clomipramine and other SSRIs are generally prescribed. While these are effective in reducing BDD symptoms, once the medication is discontinued, symptoms resume nearly immediately, suggesting this is not an effective long-term treatment option for those with BDD.

Treatment of BDD appears to be difficult, with one study finding that only 9% of clients had full remission at a 1-year follow-up, and 21% reported partial remission (Phillips, Pagano, Menard & Stout, 2006). A more recent finding reported more promising findings with 76% of participants reporting full remission over an 8-year period (Bjornsson, Dyck, et al., 2011).

5.2.5.1 Plastic surgery and medical treatments

It should not come as a surprise that many individuals with BDD seek out plastic surgery to attempt to correct their perceived defects. Phillips and colleagues (2001) evaluated treatments of clients with BDD and found that 76.4% reported some form of plastic surgery or medical treatment, with dermatology treatment the most reported (45%) followed by plastic surgery (23%). The problem with this type of treatment is that the individual is rarely satisfied with the outcome of the procedure, thus leading them to seek out additional surgeries on the same defect (Phillips, et al., 2001). Therefore, it is important that medical professionals thoroughly screen patients for BDD before completing any type of medical treatment.