ANXIETY DISORDERS, OBSESSIVE-COMPULSIVE-RELATED DISORDERS, AND TRAUMA- AND STRESS-RELATED DISORDERS
EXPECTED LEARNING OUTCOMES
After completing this chapter, the student will be able to:
1. Define anxiety
2. Identify anxiety disorders
3. Identify obsessive-compulsive-related disorders
4. Identify trauma- and stress-related disorders
5. Describe the historical perspectives and epidemiology associated with anxiety, obsessive-compulsive, and stress-related disorders
6. Discuss current scientific theories related to the etiology of anxiety, obsessive-compulsive, and stress-related disorders including relevant psychodynamic and neurobiological influences
7. Explain the various treatment options available for anxiety, obsessive-compulsive, and stress-related disorders
8. Apply the nursing process from an interpersonal perspective to the care of patients with anxiety, obsessive-compulsive, and stress-related disorders
ANXIETY is a common human emotion that is often difficult to define. Words used to describe anxiety reflect one’s inner experience and, subsequently, can be quite subjective. Typically, anxiety refers to a vague feeling involving some dread, apprehension, or other unknown tension. Life experiences teach us that anxiety can be a normal emotional response to a stressor. As a healthy response, anxiety is a catalyst to achieve, to stay focused, and to cope in threatening situations. Anxiety becomes a symptom of a disorder or pathological when it interferes with one’s ability to function. Anxiety disorders include specific phobias, panic disorders, agoraphobia, social anxiety disorders, and generalized anxiety disorder (GAD).
Obsessive-compulsive disorders (OCDs) have historically been described as a type of anxiety disorder; however, more recent findings suggest that they have a unique biological origin and are theorized by many to be solely neurologically based disorders. OCD and compulsive hoarding are discussed as subtypes of OCDs.
Trauma- and stress-related disorders, such as OCDs, were historically categorized as anxiety disorders as well. Posttraumatic stress and acute stress disorders are discussed as subtypes of trauma- and stress-related disorders.
Regardless of the specific type of disorder a person experiences, anxiety is a common factor. Persons who feel anxiety often experience somatic symptoms such as muscle pain, blurred vision, tachycardia, dyspnea, difficulty swallowing, loss of appetite, increased sweating, loss of libido, or dry mouth. Cognitive symptoms can also be manifested. These include poor memory, confusion, difficulty in concentrating, distorted thinking, unrealistic fears, repetitive fearful ideation, or hypervigilance. In addition, some people with OCDs perform certain rituals such as hand washing, counting, and so on. Persons with phobias often avoid certain situations such as large crowded areas, bridges, and elevators in order to cope with their symptoms.
Anxiety is a vague feeling of discomfort. It can be a healthy response leading an individual to become more focused and able to cope with threatening situations, or it can become pathological and interfere with a person’s ability to function.
Much has been written about the similarities and differences among FEAR, WORRY, and anxiety. For the purpose of this chapter, fear and worry are viewed as the two core symptom clusters of anxiety. Fear in this context refers to feelings consistent with panic and phobias. Worry is more indicative of symptoms such as anxious misery, apprehensive expectations, and obsessions. Anxiety, as stated earlier, is a vague, uncertain feeling of dread, whereas worry is more indicative of symptoms such as anxious misery, apprehensive expectations, and obsessions. All of the anxiety disorders maintain some form of anxiety or fear coupled with some form of worry. However, what triggers them differs (Stahl, 2013).
This chapter addresses the historical perspectives and epidemiology of anxiety, obsessive-compulsive, and trauma- and stress-related disorders (anxiety-based disorders), followed by a description of specific disorders. Scientific theories focusing on psychodynamic, behavioral, and neurobiological influences are described plus common treatment options, including pharmacotherapy and nonpharmacotherapy strategies. Application of the nursing process from an interpersonal perspective is presented, guided by the Quality and Safety Education for Nurses competencies (QSEN). Also included is a plan of care for a patient with an anxiety-based disorder.
The American Psychiatric Association (APA) did not officially recognize anxiety disorders until 1980. However, anxiety-based disorders have played substantial roles in human history. The earliest interpretations of anxiety disorders appear to be mostly spiritual, with many early spiritual treatments resembling some aspects of modern psychotherapy. For example, in early Christian thought, logismoi were distressing, obsessive thoughts that were unhealthy and believed to lead people away from God. The spiritual leaders took on roles as confessors or counselors by employing healing dialogues to lessen these obsessions. Often the treatment for logismoi was to redirect and replace unhealthy thoughts with realistic ones, which is similar to modern-day techniques of cognitive behavioral therapy (CBT). In addition, the ancient preparation and use of natural substances have similarities to modern pharmaceuticals (Anderson, 2007).
Medical interpretations of anxiety disorders are not entirely new, reaching as far back as classical Greek civilization. Greeks coined the word agoraphobic, which was initially given to people who were afraid to go outside to the market. Today this term refers to people who suffer from an anxiety disorder.
During the 17th and 18th centuries, in Germany, France, England, and North America, the term HYSTERIA (which is Greek for uterus) was used to describe anxiety and anxiety-related disorders specifically in women. During the 1800s, French psychiatrist Jean-Martin Charcot spent a great deal of energy studying hysteria and concluded that it derived from a particular hereditary disposition and was unleashed by an environmental stimulus. He postulated that certain people are genetically predisposed to develop hysteria just as today we know that there is a genetic predisposition to diseases such as cancer. Charcot observed numerous cases of hysterical symptoms arising in both men and women, including headaches, heart palpitations, chest pain, irregular pulse rate, constipation, dizziness, fainting spells, trembling of the hands and neck, emotional and sleep disorders, and mental disorientation. Although the symptoms in both men and women were similar, he believed that symptoms in men were triggered by traumatic events, such as workplace accidents and train crashes. In women, on the other hand, Charcot believed that hysterical attacks were triggered by emotions or passions such as jilted lovers and weepy, romantic girls (Porter, 1997).
In 1895, Sigmund Freud’s earliest descriptions of anxiety were documented using the term anxiety neurosis. Initially, Freud described anxiety neurosis as anxiety that resulted from a repressed libido. Later he expanded the concept of anxiety neurosis to include a diffuse sense of worry or dread that originates in a repressed thought or wish and not just in the repression of sexual energy. According to Freud, anxiety neurosis resulted in hysteria, obsessions, phobias, and somatic symptoms such as fatigue and dizziness (Sadock et al., 2014). Much of the current understanding of anxiety and anxiety-related disorders can be traced back primarily to times of war. For example, in the mid-1800s, Otto Domrich became the first in the field of medical psychology to write about anxiety attacks. This term replaced earlier notions of neurocirculatory neurasthenia, soldier’s heart, and hyperventilation syndrome that dated back to the French Revolution. These terms depicted the state of combined anxiety and cardiopulmonary symptoms that might be induced by the terrors of the battlefield (Stone, 1997).
During World War I, the number of psychiatric casualties dramatically increased such that hospitals were quickly opened to house them. According to one estimate, mental breakdowns represented 40% of British battle casualties. Military authorities attempted to hide reports of these psychiatric casualties because of their demoralizing effect on the public. Initially, the symptoms of mental breakdown were attributed to a physical cause. The British psychologist Charles Myers examined some of the first cases and attributed their symptoms to the concussive effects of exploding shells. Myers called the resulting nervous disorder “shell shock.” The name stuck, even though it soon became clear that the syndrome could be found in soldiers who had not been exposed to any physical trauma. Gradually, military psychiatrists were forced to acknowledge that the symptoms of shell shock were due to psychological trauma (Herman, 1997).
During World War II, psychiatric collapse accounted for the loss of 504,000 men from the American fighting forces. In every one of America’s wars in the 20th century, the rates of psychiatric collapse among soldiers exceeded the numbers killed in action. Psychiatric casualties constituted the single largest category of disability discharges in World War II (Gabriel, 1987).
No precise data on the number of soldiers suffering from posttraumatic stress disorder (PTSD) after the Vietnam War exist. Figures range from 500,000 to 1,500,000 PTSD cases, indicating that at least 18% and possibly as many as 54% of the armed forces suffered psychiatric symptoms. The chances that a soldier would become a psychiatric casualty in Vietnam were about the same as his or her chances of being killed in action (Gabriel, 1987). Veterans of the Gulf War, Operation Desert Shield, and Desert Storm exhibit rates of PTSD, GAD, and panic disorders that are nearly twice that of nondeployed military personnel (Black et al., 2004). Other studies have indicated that one in three Iraqi combat veterans has been diagnosed with PTSD, GAD, or a panic disorder, and one in six from Afghanistan has been diagnosed with an anxiety disorder (Milliken, Auchterlonie, & Hoge, 2007).
As research is still being done on more recent wars, it is difficult to offer specific data. This is also in part due to the fact that symptoms may begin many years after combat is over. According to Vos et al. (2012), of the 2.8 million American veterans of the Afghanistan and Iraq wars it is estimated that 11% to 20% have PTSD and of the total number of deployed Iraq and Afghanistan veterans, 118,829 were diagnosed with PTSD between 2003 and January 10, 2014.
Historically, terms such as hysteria, anxiety, neurosis, and shell shock were used to identify anxiety disorders.
In general, anxiety disorders represent the most prevalent psychiatric condition in the United States, outside of substance use disorder (Vos et al., 2012).
It is estimated that 3 out of 10 people will suffer from an anxiety disorder in their lifetime (Kessler, Berglund, Demler, Jin, & Walters, 2005). Approximately 40 million American adults aged 18 years and older, or about 18.1% of people in this age group in a given year, have an anxiety disorder. Disability common to these disorders exceeds that associated with other psychiatric conditions, as well as most medical conditions including cardiovascular disease, pulmonary disease, gastrointestinal diseases, and cancer (Merikangas et al., 2007). Despite the high prevalence rates of anxiety disorders as well as their economic burden, they often go unrecognized and untreated.
Anxiety-based disorders frequently co-occur with depressive disorders or substance abuse disorders (Kessler, Chiu, Demler, & Walters, 2005). Most people with one anxiety disorder also have another anxiety disorder. Nearly three fourths of those with an anxiety disorder will have their first episode by age 21.5 years (Kessler, Berglund, et al., 2005). The presence of any anxiety disorder is associated with a 21.9% prevalence of self-medication with drugs and alcohol. For example, persons with GAD show the highest self-medication rate of 35.6%, whereas persons with bipolar I disorder show the lowest self-medication rate of 12.6%. Caucasians are more likely to self-medicate than any other race (84.5%), and men (55.4%) are more likely to self-medicate than women (44.6%; Bolton, Cox, Clara, & Sareen, 2006).
Anxiety disorders, the most common and most costly psychiatric diagnosis in the United States, commonly occur with other conditions such as substance abuse and depression.
Statistics related to specific anxiety disorders reflect:
Approximately 6 million adults aged 18 years and older, or about 2.7% of people in this age group, have panic disorder in a given year (Kessler, Chiu, et al., 2005).
It typically develops in early adulthood, with a median age of onset of 24 years, but can extend throughout adulthood (Kessler, Bergland, et al., 2005).
About one in three people with panic disorder develops AGORAPHOBIA, a condition in which the individual becomes afraid of being in a place or situation where escape might be difficult or help unavailable in the event of a panic attack (Robins & Regier, 1991).
Approximately 2.2 million American adults aged 18 years and older, or about 1.0% of people in this age group, have OCD in a given year (Kessler, Chiu, et al., 2005).
The first symptoms of OCD often begin during childhood or adolescence.
The age of onset is 19 years (Kessler, Berglund, et al., 2005).
Approximately 7.7 million American adults aged 18 years and older, or about 3.5% of people in this age group, are diagnosed with PTSD in a given year (Kessler, Chiu, et al., 2005).
It can develop at any age, including childhood, but research shows that the median age of onset is 23 years (Kessler, Berglund, et al., 2005).
About 19% of Vietnam veterans experienced PTSD at some point after the war (Dohrenwend et al., 2006).
The disorder also frequently occurs after violent personal assaults such as rape, mugging, domestic violence, terrorism, natural or human-caused disasters, and accidents.
Approximately 6.8 million American adults, or about 3.1% of people aged 18 years and older, are diagnosed with GAD in a given year (Kessler, Chiu, et al., 2005), beginning across the life cycle with a median age of onset of 31 years (Kessler, Berglund, et al., 2005).
Approximately 15 million American adults aged 18 years and older, or about 6.8% of people in this age group, have social phobia in a given year (Kessler, Chiu, et al., 2005), typically beginning in childhood or adolescence, usually around 13 years of age (Kessler, Berglund, et al., 2005).
Approximately 1.8 million American adults aged 18 years and older, or about 0.8% of people in this age group, have agoraphobia without a history of panic disorder in a given year, with a median age of onset of 20 years (Kessler, Chiu, et al., 2005).
Approximately 19.2 million American adults aged 18 years and older, or about 8.7% of people in this age group, have some type of specific phobia (marked and persistent fear and avoidance of a specific object or situation) in a given year (Kessler, Chiu, et al., 2005), typically beginning in childhood with a median age of onset of 7 years (Kessler, Berglund, et al., 2005).
Approximately 12% of the general population suffers from social anxiety disorder (Meyer & Quenzer, 2013).
The overall prevalence of hoarding disorder is 1.5% of the population. It is significantly higher among men (4.1%) than among women (2.1%). This contrasts with the higher number of women seen in clinical practice, perhaps because many more women seek treatment (Nordsletten et al., 2013).
Those with hoarding disorder were older and more often unmarried (67%). Members of this group were also more likely to be impaired by a current physical health condition (52.6%) or comorbid mental disorder (58%; Nordsletten et al., 2013).
Morbidity and Mortality
Anxiety-based disorders, through effects of the neurological, endocrine, and immune mechanisms or direct neural stimulation that result in conditions such as hypertension or cardiac arrhythmia, can contribute to morbidity and mortality. In addition, severe anxiety disorders may be complicated by suicide, with or without secondary mood disorders (e.g., depression). Anxiety disorders have high rates of comorbidity with major depression and alcohol and drug abuse. Some of the increased morbidity and mortality associated with anxiety disorders may be related to this high rate of comorbidity.
Between 1980 and 1985, the National Institute of Mental Health (NIMH) funded the Epidemiologic Catchment Area (ECA) program of research. This program was designed to determine prevalence and incidence of mental disorders and the use of and need for services by the mentally ill. One of its findings revealed that panic disorder was associated with suicide attempts 18 times higher than populations without psychiatric disorders. The ECA study also found no difference in rates of panic disorder among White, African American, or Hispanic populations in the United States. However, some studies have found higher rates of PTSD in minority populations, which may be due to higher rates of specific traumatic events, such as assault.
The female-to-male ratio for any lifetime anxiety disorder is 3:2. It is not clear why females have higher rates of most anxiety disorders than males do. Some theories suggest that the gonadal steroids may play a role. Other research on women’s responses to stress also suggests that women experience a wider range of life events (e.g., those happening to friends) as stressful as compared with men, who react to a more limited range of stressful events, specifically only those affecting themselves or close family members (Yates, 2014).
Anxiety disorders occur more commonly in women than in men and can contribute to illness and death through effects on the endocrine, immune, and nervous system.
DESCRIPTION OF ANXIETY, OBSESSIVE-COMPULSIVE, AND TRAUMA- AND STRESS-RELATED DISORDERS
Anxiety-based disorders are common mental disorders characterized by excessive, prolonged, and debilitating levels of anxiety. They are commonly structured into the following categories based on clinical symptoms: anxiety disorders, OCDs, and trauma- and stress-related disorders.
Anxiety disorders include panic disorder, GAD, specific phobia, and social phobia.
PANIC DISORDER involves sudden, intense, and unprovoked feelings of terror and dread. In a panic attack, there is a sudden and overwhelming sense of “impending doom or a feeling that they are going to die.” People who suffer from this disorder generally develop strong fears about when and where their next panic attack will occur, and subsequently, often restrict their activities. Panic disorder usually occurs after frightening experiences or prolonged stress, but it can also occur spontaneously. A panic attack may lead an individual to be acutely aware of any change in normal body function, such as palpitations, chest pain, diaphoresis, and choking feeling.
Generalized Anxiety Disorder
GAD is a chronic disorder characterized by excessive, long-lasting anxiety and worry about nonspecific life events, objects, and situations. It differs from other anxiety-based disorders in that there is pervasive cognitive dysfunction, impaired functioning, and poor health-related outcomes (Varcarolis, 2015). People with GAD often feel afraid and worry about health, money, family, work, or school, but have trouble both in identifying the specific fear and in controlling the worries. Their fear is typically out of proportion with what may be expected in their situation. They expect failure and disaster to the point that it interferes with daily functions like work, school, social activities, and relationships. People with GAD have recurring fears or worries about health or finances, and they often have a persistent sense that something bad is about to happen. The reason for the intense feelings of anxiety may be difficult to identify. However, the fears and worries are very real and often keep individuals from concentrating on daily tasks.
Although panic disorder can occur spontaneously, it typically results after frightening experiences or prolonged stress. Patients with OCD use obsessions and compulsions to relieve anxiety. Patients with PTSD experience flashbacks and change behavior in an effort to avoid stimuli associated with a previous trauma.
PHOBIAs are intense fears about certain objects or situations. Specific phobias may involve things such as encountering certain animals or flying in airplanes. One example is agoraphobia. Agoraphobia involves intense fear and anxiety of any place or situation where escape might be difficult, leading to avoidance of situations such as being alone outside of the home; traveling in a car, bus, or airplane; or being in a crowded area (Kessler, Berglund, et al., 2005). Individuals will situate themselves so that escape will not be difficult or embarrassing. Additionally, they will change their behavior to reduce anxiety about being able to escape.
Social phobia is a type of phobia characterized by a fear of being negatively judged by others or a fear of public embarrassment due to impulsive actions. This includes feelings such as stage fright, fear of intimacy, and fear of humiliation. This disorder can cause people to avoid public situations and human contact to the point that normal life is rendered impossible.
These disorders include Obsessive-compulsive disorder (OCD), hoarding disorder, and body dysmorphic disorder (BDD).
OCD is an anxiety disorder characterized by thoughts or actions that are repetitive, distressing, and intrusive. People with OCD usually know that their compulsions are unreasonable or irrational, but they serve to alleviate their anxiety. Often, the logic of someone with OCD will appear superstitious, such as an insistence to walk in a certain pattern. People with OCD may obsessively clean personal items or hands or constantly check locks, light switches, and so on (APA, 2013).
Persons with hoarding disorder have difficulty discarding or parting with possessions due to strong urges to save the items. Difficulty discarding often includes items that others consider to be of little use and results in accumulation of a large number of possessions that clutter the home, preventing use for the intended purpose. They often are not able to sleep in their bed, sit in their living room, or cook in their kitchen. They may hold on to items due to the perceived usefulness, aesthetic value, or for sentimental reasons. For the patient with hoarding disorder, the prospect of parting with possessions causes significant distress (Hartmann, Blashill, Greenberg, Wilhelm, Storch, & McKay, 2014).
Body Dysmorphic Disorder (BDD)
BDD is characterized by a preoccupation with an imagined or slight defect in appearance. These concerns can involve any body area, however, they are typically focused on the face and head. These concerns often become obsessive in nature, consuming significant time, and are difficult to resist and control. In some patients, insight is poor and they may have difficulty realizing that they look normal (APA, 2013).
Trauma- and Stress-Related Disorders
Trauma- and stress-related disorders include posttraumatic stress disorder (PTSD) and acute stress disorder.
Posttraumatic Stress Disorder
PTSD results from previous trauma such as military combat, rape, hostage situations, or a serious accident. PTSD often leads to flashbacks and behavioral changes in order to avoid certain stimuli. Thoughts, feelings, and behavior patterns become seriously affected by reminders of the event, sometimes months or even years after the traumatic experience (APA, 2013).
Acute Stress Disorder
Acute stress disorder occurs when a person has been exposed to a traumatic event or experience involving intense fear, horror, or helplessness. It is labeled acute because it refers to the anxiety and behavioral disturbances that develop and are alleviated within the first month after exposure to an extreme trauma. The event or experience must involve a threat of death, serious injury, or physical integrity. The event or experience may be to the person themselves or to others around them (APA, 2013).
The exact etiology of anxiety disorders is not known. Numerous research studies have attempted to address the underlying causes of anxiety, but without success.
Two psychosocial influences dominate the thinking related to the development of anxiety disorders. These are the psychodynamic influences of theorists such as Sigmund Freud, Harry Sullivan, and Hildegard Peplau, and behavioral and learning theories.
In 1894, Sigmund Freud first published his writings on the psychodynamic nature of anxiety. His last publication on the topic was in 1926. According to Freud, the conflicting demands among the id, ego, and superego produce anxiety. He described anxiety as a signal to the ego that an unacceptable drive was pressing for conscious representation or discharge. For example, when the ego blocks the pleasurable desires of the id, anxiety is felt. This diffuse, distressed state develops when the ego senses that the id is going to cause harm to the individual. Freud identified three types of anxiety:
Reality anxiety: The most basic form, rooted in reality such as fear of a bee sting or fear felt just before an accident; also referred to as ego-based anxiety.
Neurotic anxiety: Arising from an unconscious fear that the libidinal impulses of the id will take control at an inopportune time; driven by a fear of punishment that will result from expressing the id’s desires without proper sublimation.
Moral anxiety: Resulting from fear of violating moral or societal codes; appearing as guilt or shame.
Freud believed that when anxiety is present, it alerts the ego to resolve the conflict by means of defense mechanisms. (See Chapter 10 for a more in-depth discussion of defense mechanisms.) Of all the defense mechanisms, Freud believed that repression is the most powerful and pervasive defense mechanism working to push unacceptable id impulses out of awareness and back into the unconscious mind. Repression is the foundation from which all other defense mechanisms work. The goal of every defense mechanism is to repress, or push threatening impulses out of awareness. Freud said that our early childhood experiences, many of which he believed are sexually laden, are too threatening and stressful for us to deal with consciously. Individuals then reduce the anxiety of this conflict through the defense mechanism of repression (Freud, 1938).
Freud’s pupil and later critic, Otto Rank, separated from Freud by describing anxiety as a result of birth trauma. According to Rank, the anxiety experienced during birth was the model for all anxiety experienced afterward. While he viewed anxiety as trauma from birth, another theorist, Harry Stack Sullivan, believed anxiety stemmed from the early relationship between the mother and the child and the transmission of the mother’s anxiety to the infant.
Sullivan called his approach an interpersonal theory of psychiatry because he believed psychiatry is the study of what goes on between people. This is in contrast to Freud’s paradigm that focused on what goes on inside people. Freud’s is a drive model whereas Sullivan’s is an interpersonal model.
For Sullivan, relationships are primary. Personality is a hypothetical entity that cannot be observed or studied apart from interpersonal situations. The only way personality can be known is through the medium of interpersonal interactions. Therefore, what is to be studied is not the individual person, but the interpersonal situation.
Like Sullivan, Hildegard Peplau (1991) also believed that relationships are primary. She applied psychodynamic theories not only to individuals but also to the nursing process. She clearly illustrated in her writings and teaching that she felt nursing was a significant and therapeutic, interpersonal process. Peplau wrote extensively about unexplained discomfort and within these writings described four types of anxiety:
Mild anxiety: This anxiety motivates individuals every day; it is considered “normal anxiety” and viewed as a positive motivator for personal growth and success.
Moderate anxiety: The individual begins to hear, see, and grasp less due to a narrowing of his or her perceptual field; decreased awareness of the environment and decreased focus, noticing only those things that are brought to the individual’s attention.
Severe anxiety: The individual’s thoughts become scattered, focusing on small details; inability to problem solve or use the learning process to make decisions.
Panic: The individual experiences intense fear accompanied by physical symptoms such as chest pain, heart palpitations, dizziness, shortness of breath, and abdominal distress; possible inability to cooperate or collaborate with the nurse.
Peplau believed that clearly identifying and understanding the type of anxiety an individual is experiencing are pivotal for good nursing care. She believed that nursing interventions were not required during mild episodes of anxiety. For moderate levels of anxiety, Peplau believed many useful nursing interventions could take place such as problem-solving/talk therapy, cognitive reframing, and teaching anxiety-reduction techniques such as relaxation training, meditation, counting, and deep breathing. During periods of severe anxiety, Peplau suggested that individuals cannot effectively problem solve or make connections because they are self-absorbed, feeling an impending sense of doom, and experiencing physiological symptoms such as hyperventilation and tachycardia. Nursing interventions during this time focus on providing short, firm concrete directions to assist the person to remain calm, to protect the person from self-injury, either intentional or related to inattention or poor reality testing, and to protect the milieu from disruption and injury.
Peplau postulated that persons with panic levels of anxiety were unable to focus on even one detail within the environment. She believed that terror, emotional paralysis, hallucinations, or delusions might occur during panic. Individuals can become mute, extremely agitated, irrational, hypervigilant, and hyperactive. When a person experiences panic, Peplau suggested that the nurse should remain with the individual until the panic subsides. This action provides a certain amount of security, or “thereness” of the nurse.
Peplau identified four categories of anxiety: mild, moderate, severe, and panic.
Before more recent biological and pharmacological studies about anxiety, the widely accepted theory of anxiety disorders fell within behavioral or learning theories. Although Freud was working on the psychodynamics of anxiety, a radically different view of anxiety and fear, significantly influenced by Pavlov’s theory of classical conditioning (1927), was emerging through the work of Watson and Morgan (1917). They argued that anxiety was a conditioned response to an unpleasant stimulus. This theory, also known as respondent conditioning, was disregarded by many. However, it laid the groundwork for cognitive and social-learning theories of anxiety and has undergone considerable transformation. These theories primarily focused on simple phobias and fears. Thus, the concepts of classical conditioning were not adequate to explain more complex anxiety states. Most learning and behavioral theorists now embrace interactive models that attempt to explain the multifaceted nature of anxiety disorders. These models take into account how individual risk factors interact with environmental factors to produce anxiety states or disorders. For example, an interactive model of anxiety would suggest that individuals with controlling, time conscious, and impatient personality (type A) would be more prone to anxiety in a highly chaotic or stressful work environment (Taylor & Arnow, 1988).
Most biological theories regarding anxiety-based disorders focus primarily on neurostructural and neurochemical influences. However, these disorders are complex diseases that are also caused by a combination of genetic and environmental factors.
The anxiety-based disorders are so broad that the neurobiology that seems most relevant in one anxiety disorder may have little to do with other anxiety disorders. As stated earlier, all of these disorders seem to have the core feature of fear and/or worry. More than ever, there is a plethora of research regarding the neurocircuitry and neurochemistry associated with anxiety disorders, OCDs, and trauma- and stress-related disorders. Although scientific evidence of anxiety disorders continues to be rooted in symptoms of anxiety and fear, there are discrete differences in the neurobiology of OCDs such as hoarding and trauma- and stress-related disorders such as posttraumatic stress syndrome.
Neurobiological Influences of Anxiety Disorders
Symptoms of anxiety or fear are associated with the malfunctioning of amygdala-centered circuits. The amygdala is an almond-shaped structure in the brain located near the hippocampus. It has anatomical connections that allow it to integrate sensory and cognitive information and then determine whether there will be a fear response. In contrast to fear, symptoms of worry such as anxious misery, apprehension, catastrophic thinking, and obsessions are linked to the cortico-striatal–thalamic–cortical (CSTC) loop circuitry. Both the amygdala and the CSTC loops contain gamma-amino-butyric acid (GABA), norepinephrine, and serotonin as the main neurotransmitters. Other neurotransmitters and peptides, such as dopamine, glutamate (a precursor to GABA), and corticotropin-releasing factor (CRF), have also been studied as playing a role in the development of anxiety symptoms. In addition, voltage-gated ion channels are involved in neurotransmission within these circuits (Stahl, 2013).
GABA is the main neurotransmitter involved in anxiety responses and in the anxiolytic action of many of the medications used to treat anxiety disorders. It directly influences an individual’s personality and ability to handle stress. GABA is an inhibitory neurotransmitter that plays a regulatory role in reducing the activity of many neurons, including those in the amygdala and the CSTC loop, which affects one’s sense of worry. It acts as the primary calming, or “peacemaker,” chemical, inducing relaxation, reducing stress and anxiety, and increasing alertness. Overactivation or malfunction of the amygdala circuits leads to pathological anxiety or fear. GABA-ergic agents such as benzodiazepines act at postsynaptic GABA receptors to enhance the inhibitory action of GABA, thus decreasing the fear or anxiety symptoms.
As stated previously, anxiety disorders frequently co-occur with depressive disorders. Anxiety and depressive disorders also share symptoms, brain circuits, and neurotransmitters. Recall from Chapter 12 that altered levels of the neurotransmitter, serotonin, have been implicated in depressive disorders. It has also been postulated that serotonin works to decrease anxiety symptoms because it works in the amygdala to regulate the vulnerability of fear circuits (Stahl, 2013). Studies show that certain antidepressants increase the amount of available serotonin by blocking its reuptake. These medications have proven efficacious for anxiety disorders as well.
Neurobiological Influences of OCDs
The anterior cingulated cortex is part of the limbic system in the brain. Persons who hoard exhibit dysfunction in the anterior cingulate cortex (ACC) and associated frontal and medial areas. The dorsal ACC is postulated to be involved in decision making, error monitoring, and reward-based learning. The ventral ACC is thought to aid in assigning emotional and motivational meaning to stimuli and experiences. It is unsurprising that hoarding disorder, which is characterized by the inability to make decisions due to error vigilance and overwhelming emotions, might be associated with dysfunction in these regions (Bush, Luu, & Posner, 2000).
Neurobiological Influences of Trauma- and Stress-Related Disorders
Norepinephrine, the neurotransmitter often associated with the “fight or flight” response to stress, also has regulatory input to the amygdala. This neurotransmitter is strongly linked to physical responses and reactions, including increasing heart rate and blood pressure as well as creating a sense of panic and overwhelming fear or dread. Excessive output of norepinephrine from the locus coeruleus results not only in autonomic overdrive but also can trigger symptoms of anxiety and fear, nightmares, hyperarousal states, flashbacks, and panic attacks. Blocking alpha-1- and beta-1-adrenergic receptors within the amygdala leads to a lessening of these symptoms. This is why beta-blockers such as propranolol and, more recently, alpha-1-adrenergic blockers such as prazosin (Minipress) have been used to treat anxiety symptoms (Stahl, 2013).
Additionally, the brain structures that are functionally altered in PTSD patients largely overlap with circuits that are responsible for fear learning and expression (Shin & Handwerger, 2009; Van Elzakker, Dahlgren, Davis, Dubois, & Shin, 2014). As such, knowing how specific neuronal circuits support associative learning during aversive or traumatic events, their role in the generation and regulation of fear- and anxiety-related behaviors in the presence of trauma-related stimuli, is essential for an understanding of the development of anxiety disorders.
Specific brain structures such as the amygdala and neurotransmitters such as GABA, norepinephrine, and serotonin have been associated with anxiety disorders. GABA is the primary neurotransmitter involved.
The study of genetic vulnerability or the idea that a person may have a biological predisposition to develop a disorder when certain environmental factors present themselves has been gaining attention within the psychiatric arena. Of the known risk factors for anxiety disorders, the most validated is family history. Family and twin studies have demonstrated that anxiety-based disorders have significant familial aggregation, and their heritability estimates range from 30% to 50% (Hettema, Neale, & Kendler, 2001).
Smoller, Block, and Young (2009) reported that genetic epidemiological studies have clearly shown that all of the anxiety disorders aggregate in families and that familiality is primarily due to genetic factors. Interestingly, studies of temperament since the 1950s have concluded that temperamental differences in individuals have a biological or genetic basis, particularly in regard to fear and stress reactions.
For example, psychologist Jerome Kagan has demonstrated that people born with a certain brain circuitry also have a “hyperreactive amygdala.” He reports that infants born with this vulnerability have a “high reactivity” when exposed to new stimuli and later become inhibited, shy, and anxious adults (Henig, 2009). Other researchers have found that elevated anxious temperament is associated with decreased messenger RNA expression of two neuropeptide Y receptors, Y1R and Y5R, in the central nucleus of the amygdala, a region of the brain that plays an important role in regulating fear and anxiety (Roseboom et al., 2014).
Psychiatrist Stephen Stahl (2013) discussed the idea that there are vulnerable circuits in the brain that are created by certain genes. These circuits, when stressed by environmental factors such as childhood sexual abuse, can lead to anxiety disorders later in life. Genome-wide association studies (GWAS) have proven to be a successful method for the identification of common genetic variants that increase susceptibility to complex diseases or traits. Recently, several GWAS of anxiety-based disorders such as panic disorder, OCDs, phobias, and PTSDs have been published (Otowa et al., 2014).
Various treatment options are available for anxiety disorders. Anxiety disorders will most likely require concomitant use of nonpharmacological and pharmacological strategies. Studies show that for many patients, a combination of medication and cognitive behavioral/exposure therapy was shown to be a clinically desired treatment strategy (Bandelow et al., 2012).
Pharmacological therapy for anxiety disorders is similar to that for depression. Specifically, selective serotonin reuptake inhibitors (SSRIs) and selective norepinephrine reuptake inhibitors (SNRIs) are the drugs of choice for treating both depressive disorders and anxiety disorders. Patients need to understand that the therapeutic anxiolytic effects of SSRIs and SNRIs range from approximately 2 to 8 weeks, but more commonly, 6 to 8 weeks. This time frame is typically longer than what is seen when used to treat depression. Also, higher doses of SSRIs are required to treat anxiety symptoms when compared with depression symptoms. Drug Summary 13-1 highlights the major medications commonly used to treat anxiety disorders. Different combinations of pharamacological agents may be used depending on the specific anxiety disorder.
Generalized Anxiety Disorder
Both SSRIs, generally prescribed in higher doses, and SNRIs, typically prescribed in usual doses, are considered first-line treatment for GAD. However, due to the serotonergic properties of SSRIs and SNRIs, some individuals report feeling more anxious and excited instead of feeling calm. Because these agents have a delayed onset of action, benzodiazepines are often prescribed concurrently when initiating treatment. Benzodiazepines are also used when there is only a partial response to an SSRI or SNRI or for intermittent use when anxiety symptoms worsen and quick relief is required (Stahl, 2013). Another first-line agent for treating GAD is buspirone (BuSpar), used alone or as an adjunct to SSRIs or SNRIs. (See Chapter 12 for an expanded discussion of SSRIs and SNRIs.)
If a patient does not respond to initial treatment choices, switching to an agent within the same class is often considered. When a patient fails to respond to any first-line treatment, trials of mirtazapine (Remeron), trazodone (Desyrel), tricyclic antidepressants, or sedating antihistamines such as hydroxyzine (Vistaril) may be used. Other second-line agents may include the novel alpha-2 delta ligands, gabapentin (Neurontin), or pregabalin (Lyrica). These drugs are approved for seizures, neuropathic pain, and fibromyalgia. Currently, they are being tested as treatment for anxiety disorders (Stahl, 2013). Atypical antipsychotics are often used as adjunct treatment in patients that have severe refractory and disabling symptoms that are unremitting. (See Chapter 12 for a more detailed discussion of tricyclic antidepressants; see Chapter 11 for a more detailed discussion of antipsychotics.)
Treatment for panic disorders is similar to that for GAD. SSRIs, generally prescribed in doses higher than for treating depression, and SNRIs, prescribed in usual doses, are considered first-line treatment. Benzodiazepines are used when there is only partial response to an SSRI or SNRI or for intermittent use. They are also used alone as first-line treatment when symptoms are acute, severe, and disabling.
Second-line treatment may include the novel alpha-2 delta ligands, gabapentin, or pregabalin. Occasionally, mirtazapine and trazodone are used alone or to augment therapy with SSRIs and/or SNRIs. Often, tricyclic antidepressants (TCAs) are used and the monoamine oxidase inhibitors (MAOIs), although commonly avoided due to their unfavorable side-effect profile, are particularly efficacious in the treatment of panic disorders (Stahl, 2013). Other adjunctive treatments include the use of atypical antipsychotics such as quetiapine (Seroquel) and olanzapine (Zyprexa), and anticonvulsants such as lamotrigine (Lamictal) and topiramate (Topamax). (See Chapter 12 for a more in-depth discussion of MAOIs.)
High doses of SSRIs are considered first-line treatment for OCD. Commonly, two or three different SSRIs at high doses are tried if the first SSRI is not effective. Second-line agents include clomipramine (Anafranil) and SNRIs, particularly venlafaxine (Effexor; Dell’Osso, Nestadt, Allen, & Hollander, 2006) and MAOIs. If a patient responds only partially or does not respond to SSRI therapy, atypical antipsychotics may be used for augmentation. Risperidone (Risperdal) is considered a first-line agent for such augmentation (Fineberg & Gale, 2005). Additionally, atypical antipsychotic agents are the only established agents for treating SSRI-refractory OCD (Keuneman, Pokos, Weerasundera, & Castle, 2005). Other pharmacological options for refractory OCD based on limited research data include intravenous clomipramine and citalopram (Celexa), as well as combined SSRI–clomipramine treatment.
Many other drugs have been studied in OCD treatment. Opioid agonists such as tramadol hydrochloride (Ultram) and morphine have shown encouraging results. These drugs inhibit glutamate release in the cerebral cortex, disinhibit serotonergic neurons in the dorsal raphe, and increase dopamine transmission in the striatum leading to a decrease in distressing, obsessional thoughts, and a reduction in compulsive actions. In addition, glutamate (MSG) has been cited as a novel treatment target. Drugs such as riluzole (Rilutek), memantine (Namenda), and N-acetylcysteine, which lessen glutamatergic transmission, have shown encouraging results. However, more research is needed (Lafleur et al., 2006).
Body Dysmorphic Disorder
There has been a growing recognition that BDD is common, and is associated with significant illness and disability. There is also some evidence that it may respond to pharmacotherapy and psychotherapy. Although few, small, controlled trials have been conducted, the results suggest that treatment with both medication (SSRIs) or psychotherapy can be effective in treating the symptoms of BDD (Ipser, Sander, & Stein, 2009).