Abnormal Psychology: Anxiety, Trauma, and Related Disorders - Barlow (PDF)
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Summary
This document reviews anxiety, trauma, and stressor-related disorders, covering biological and psychological perspectives, as well as treatment approaches. It discusses panic attacks, generalized anxiety disorder, and agoraphobia, examining various contributors to these conditions. The document is focused on abnormal psychology and not an exam paper.
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Anxiety, Trauma- and Stressor-Related, and Obsessive-Compulsive and Related Disorders Anxiety is a negative mood state characterized by bodily symptoms of physical tension and by apprehension about the future. Social, physical, and intellectual performances are driven and enhanced by anxiet...
Anxiety, Trauma- and Stressor-Related, and Obsessive-Compulsive and Related Disorders Anxiety is a negative mood state characterized by bodily symptoms of physical tension and by apprehension about the future. Social, physical, and intellectual performances are driven and enhanced by anxiety. Fear is an immediate emotional reaction to current danger characterized by strong escapist action tendencies and, often, a surge in the sympathetic branch of the autonomic nervous system. Panic Attack In psychopathology, a panic attack is defined as an abrupt experience of intense fear or acute discomfort, accompanied by physical symptoms that usually include heart palpitations, chest pain, shortness of breath, and, possibly, dizziness. Two basic types of panic attacks are described in DSM-5: expected and unexpected. Unexpected attacks are important in panic disorder. Expected attacks more common in specific phobias or social phobia. If you know you are afraid of high places or of driving over long bridges, you might have a panic attack in these situations but not anywhere else; this is an expected (cued) panic attack. By contrast, you might experience unexpected (uncued) panic attacks if you don’t have a clue when or where the next attack will occur. Biological Contributions As with almost all emotional traits and psychological disorders, no single gene seems to cause anxiety or panic. Instead, contributions from collections of genes in several areas on chromosomes make us vulnerable when the right psychological and social factors are in place. Depleted levels of gammaaminobutyric acid (GABA), part of the GABA–benzodiazepine system, are associated with increased anxiety, although the relationship is not quite so direct. The noradrenergic system has also been implicated in anxiety, and evidence from basic animal studies, as well as studies of normal anxiety in humans, suggests the serotonergic neurotransmitter system is also involved. But increasing attention in the last several years is focusing on the role of the corticotropin-releasing factor (CRF) system as central to the expression of anxiety (and depression) and the groups of genes that increase the likelihood that this system will be turned on. This is because CRF activates the hypothalamic– pituitary–adrenocortical (HPA) axis, which is part of the CRF system, and this CRF system has wide-ranging effects on areas of the brain implicated in anxiety, including the emotional brain (the limbic system), particularly the hippocampus and the amygdala; the locus coeruleus in the brain stem; the prefrontal cortex; and the dopaminergic neurotransmitter system. The CRF system is also directly related to the GABA–benzodiazepine system and the serotonergic and noradrenergic neurotransmitter systems. The area of the brain most often associated with anxiety is the limbic system which acts as a mediator between the brain stem and the cortex. The more primitive brain stem monitors and senses changes in bodily functions and relays these potential danger signals to higher cortical processes through the limbic system. The late Jeffrey Gray, a prominent British neuropsychologist, identified a brain circuit in the limbic system of animals that seems heavily involved in anxiety. The system that Gray calls the behavioral inhibition system (BIS). BIS is activated by signals from the brain stem of unexpected events, such as major changes in body functioning that might signal danger. Danger signals in response to something we see that might be threatening descend from the cortex to the septal–hippocampal system. The BIS also receives a big boost from the amygdala. When the BIS is activated by signals that arise from the brain stem or descend from the cortex, our tendency is to freeze, experience anxiety, and apprehensively evaluate the situation to confirm that danger is present. The BIS circuit is distinct from the circuit involved in panic. Gray and Graeff identified what Gray calls the fight/flight system (FFS). This circuit originates in the brain stem and travels through several midbrain structures, including the amygdala, the ventromedial nucleus of the hypothalamus, and the central gray matter. When stimulated in animals, this circuit produces an immediate alarm-and-escape response that looks very much like panic in humans. The FFS is activated partly by deficiencies in serotonin, suggest Gray and McNaughton. One important study suggested that cigarette smoking as a teenager is associated with greatly increased risk for developing anxiety disorders as an adult, particularly panic disorder and generalized anxiety disorder. Psychological Contributions Freud thought anxiety was a psychic reaction to danger surrounding the reactivation of an infantile fearful situation. Behavioral theorists thought anxiety was the product of early classical conditioning, modeling, or other forms of learning. A general “sense of uncontrollability” may develop early as a function of upbringing and other disruptive or traumatic environmental factors. Parents who provide a “secure home base” but allow their children to explore their world and develop the necessary skills to cope with unexpected occurrences enable their children to develop a healthy sense of control. Social Contributions Stressful life events trigger our biological and psychological vulnerabilities to anxiety. Most are social and interpersonal in nature—marriage, divorce, difficulties at work, death of a loved one, pressures to excel in school, and so on. Some might be physical, such as an injury or illness. DSM-5 now makes it explicit that panic attacks often co-occur with certain medical conditions, particularly cardio, respiratory, gastrointestinal, and vestibular (inner ear) disorders, even though the majority of these patients would not meet criteria for panic disorder. Based on epidemiological data, Weissman and colleagues found that 20% of patients with panic disorder had attempted suicide. Generalized Anxiety Disorder The DSM-5 criteria specify that at least 6 months of excessive anxiety and worry (apprehensive expectation) must be ongoing more days than not. Whereas panic is associated with autonomic arousal, presumably as a result of a sympathetic nervous system surge (for instance, increased heart rate, palpitations, perspiration, and trembling), GAD is characterized by muscle tension, mental agitation, susceptibility to, fatigue (probably the result of chronic excessive muscle tension), some irritability, and difficulty sleeping. Focusing one’s attention is difficult, as the mind quickly switches from crisis to crisis. Statistics About two-thirds of individuals with GAD are female in both clinical samples. But this sex ratio may be specific to developed countries. In the South African study mentioned here, GAD was more common in males. Some people with GAD report onset in early adulthood, usually in response to a life stressor. The median age of onset based on interviews is 31. GAD is prevalent among older adults. In the large national comorbidity study and its replication, GAD was found to be most common in the group over 45 years of age and least common in the youngest group, ages 15 to 24. Treatment Benzodiazepines are most often prescribed for generalized anxiety, and the evidence indicates that they give some relief, at least in the short term. Furthermore, benzodiazepines carry some risks. First, they seem to impair both cognitive and motor functioning. Specifically, people don’t seem to be as alert on the job or at school when they are taking benzodiazepines. The drugs may impair driving, and in older adults they seem to be associated with falls, resulting in hip fractures. More important, benzodiazepines seem to produce both psychological and physical dependence, making it difficult for people to stop taking them. There is stronger evidence for the usefulness of antidepressants in the treatment of GAD, such as paroxetine (also called Paxil) and venlafaxine (also called Effexor). In the early 1990s, we developed a cognitive-behavioral treatment (CBT) for GAD in which patients evoke the worry process during therapy sessions and confront anxiety-provoking images and thoughts head-on. CBT and the antidepressant drug sertraline (Zoloft) were equally effective immediately following treatment compared with taking placebo pills for children with GAD and other related disorders. Panic Disorder and Agoraphobia Panic disorder (PD), in which individuals experience severe, unexpected panic attacks; they may think they’re dying or otherwise losing control. In many cases but not all, PD is accompanied by a closely related disorder called agoraphobia, which is fear and avoidance of situations in which a person feels unsafe or unable to escape to get home or to a hospital in the event of a developing panic symptoms or other physical symptoms, such as loss of bladder control. In DSM-IV, panic disorder and agoraphobia were integrated into one disorder called panic disorder with agoraphobia, but investigators discovered that many people experienced panic disorder without developing agoraphobia and some people develop agoraphobia in the absence of panic disorder. Many people who have panic attacks do not necessarily develop panic disorder. To meet criteria for panic disorder, a person must experience an unexpected panic attack and develop substantial anxiety over the possibility of having another attack or about the implications of the attack or its consequences. A few individuals do not report concern about another attack but still change their behavior in a way that indicates the distress the attacks cause them. They may avoid going to certain places or neglect their duties around the house for fear an attack might occur if they are too active. The term agoraphobia was coined in 1871 by Karl Westphal, a German physician, and, in the original Greek, refers to fear of the marketplace. Most agoraphobic avoidance behavior is simply a complication of severe, unexpected panic attacks. We know that anxiety is diminished for individuals with agoraphobia if they think a location or person is “safe”, even if there is nothing effective the person could do if something bad did happen. Agoraphobic avoidance seems to be determined for the most part by the extent to which you think or expect you might have another attack rather than by how many attacks you actually have or how severe they are. Thus, agoraphobic avoidance is simply one way of coping with unexpected panic attacks. Other methods of coping with panic attacks include using (and eventually abusing) drugs and/or alcohol. Some individuals do not avoid agoraphobic situations but endure them with “intense dread.” Most patients with panic disorder and agoraphobic avoidance also display another cluster of avoidant behaviors that we call interoceptive avoidance, or avoidance of internal physical sensations. These behaviors involve removing oneself from situations or activities that might produce the physiological arousal that somehow resembles the beginnings of a panic attack. Some patients might avoid exercise because it produces increased cardiovascular activity or faster respiration, which reminds them of panic attacks and makes them think one might be beginning. Other patients might avoid sauna baths or any rooms in which they might perspire. Statistics PD is fairly common. Approximately 2.7% of the population meet criteria for PD during a given 1-year period and 4.7% met them at some point during their lives, two-thirds of them women. Onset of panic disorder usually occurs in early adult life—from midteens through about 40 years of age. The median age of onset is between 20 and 24. Important work on anxiety in the elderly suggests that health and vitality are the primary focus of anxiety in the elderly population. As we have said, most (75% or more) of those who suffer from agoraphobia are women. For a long time, we didn’t know why, but now it seems the most logical explanation is cultural. It is more accepted for women to report fear and to avoid numerous situations. Men, however, are expected to be stronger and braver, to “tough it out.” Men consume large amounts of alcohol. The problem is that they become dependent on alcohol, and many begin the long downward spiral into serious addiction. Approximately 60% of the people with panic disorder have experienced such nocturnal attacks. In fact, panic attacks occur more often between 1:30 a.m. and 3:30 a.m. than any other time. In some cases, people are afraid to go to sleep at night. Causes Clark emphasizes the specific psychological vulnerability of people with this disorder to interpret normal physical sensations in a catastrophic way. In other words, although we all typically experience rapid heartbeat after exercise, if you have a psychological or cognitive vulnerability, you might interpret the response as dangerous and feel a surge of anxiety. One hypothesis that panic disorder and agoraphobia evolve from psychodynamic causes suggested that early object loss and/or separation anxiety might predispose someone to develop the condition as an adult. Dependent personality tendencies often characterize a person with agoraphobia. These characteristics were hypothesized as a possible reaction to early separation. Treatment A large number of drugs affecting the noradrenergic, serotonergic, or GABA–benzodiazepine neurotransmitter systems, or some combination, seem effective in treating panic disorder. Including high-potency benzodiazepines, the newer selective-serotonin reuptake inhibitors (SSRIs) such as Prozac and Paxil. And the closely related serotonin-norepinephrine reuptake inhibitors (SNRIs), such as venlafaxine. SSRIs are currently the indicated drug for panic disorder based on all available evidence, although sexual dysfunction seems to occur in 75% or more of people taking these medications. On the other hand, high-potency benzodiazepines such as alprazolam (Xanax), commonly used for panic disorder, work quickly but are hard to stop taking because of psychological and physical dependence and addiction. The strategy of exposure-based treatments is to arrange conditions in which the patient can gradually face the feared situations and learn there is nothing to fear. Gradual exposure exercises, sometimes combined with anxiety-reducing coping mechanisms such as relaxation or breathing retraining, have proved effective in helping patients overcome agoraphobic behavior whether associated with panic disorder or not. Panic control treatment (PCT) developed at one of our clinics concentrates on exposing patients with panic disorder to the cluster of interoceptive (physical) sensations that remind them of their panic attacks. The therapist attempts to create “mini” panic attacks in the office by having the patients exercise to elevate their heart rates or perhaps by spinning them in a chair to make them dizzy. General conclusions from these studies suggest no advantage to combining drugs and CBT initially for panic disorder and agoraphobia. Furthermore, the psychological treatments seemed to perform better in the long run (6 months after treatment had stopped). This suggests the psychological treatment should be offered initially, followed by drug treatment for those patients who do not respond adequately or for whom psychological treatment is not available. Specific Phobia A specific phobia is an irrational fear of a specific object or situation that markedly interferes with an individual’s ability to function. Four major subtypes of specific phobia have been identified: blood–injection–injury type situational type (such as planes, elevators, or enclosed places) natural environment type (for example, heights, storms, and water) and animal type A fifth category, “other,” includes phobias that do not fit any of the four major subtypes (for example, situations that may lead to choking, vomiting, or contracting an illness or, in children, avoidance of loud sounds or costumed characters). Those with blood–injection–injury phobias almost always differ in their physiological reaction from people with other types of phobia. The average age of onset for this phobia is approximately 9 years. Phobias characterized by fear of public transportation or enclosed places are called situational phobias. Claustrophobia, a fear of small enclosed places, is situational, as is a phobia of flying. The main difference between situational phobia and panic disorder is that people with situational phobia never experience panic attacks outside the context of their phobic object or situation. Therefore, they can relax when they don’t have to confront their phobic situation. Sometimes very young people develop fears of situations or events occurring in nature. These fears are called natural environment phobias. The major examples are heights, storms, and water. In any case, these phobias have a peak age of onset of about 7 years. They are not phobias if they are only passing fears. They have to be persistent (lasting at least six months) and to interfere substantially with the person’s functioning, leading to avoidance of boat trips or summer vacations in the mountains where there might be a storm. Fears of animals and insects are called animal phobias. Again, these fears are common but become phobic only if severe interference with functioning occurs. The age of onset for these phobias, like that of natural environment phobias, peaks around 7 years. Statistics Not surprisingly, fears of snakes and heights rank near the top. Notice also that the sex ratio among common fears is overwhelmingly female with a couple of exceptions. Among these exceptions is fear of heights, for which the sex ratio is approximately equal. As with common fears, the sex ratio for specific phobias is, at 4:1, overwhelmingly female; this is also consistent around the world. The median age of onset for specific phobia is 7 years of age, the youngest of any anxiety disorder except separation anxiety disorder. Specific phobias seem to decline with old age. Causes An individual with claustrophobia who recently came to our clinic reported being trapped in an elevator for an extraordinarily long period. These are examples of phobias acquired by direct experience, where real danger or pain results in an alarm response (a true alarm). This is one way of developing a phobia, and there are at least three others: experiencing a false alarm (panic attack) in a specific situation, observing someone else experience severe fear (vicarious experience), or, under the right conditions, being told about danger. Treatment Almost everyone agrees that specific phobias require structured and consistent exposure-based exercises. Nevertheless, most patients who expose themselves gradually to what they fear must be under therapeutic supervision. Individuals who attempt to carry out the exercises alone often attempt to do too much too soon and end up escaping the situation, which may strengthen the phobia. For separation anxiety, parents are often included to help structure the exercises and also to address parental reaction to childhood anxiety. Separation Anxiety Disorder Separation anxiety disorder is characterized by children’s unrealistic and persistent worry that something will happen to their parents or other important people in their life or that something will happen to the children themselves that will separate them from their parents (for example, they will be lost, kidnapped, killed, or hurt in an accident). Children often refuse to go to school or even to leave home, not because they are afraid of school but because they are afraid of separating from loved ones. All young children experience separation anxiety to some extent; this fear usually decreases as they grow older. It is also important to differentiate separation anxiety from school phobia. In school phobia, the fear is clearly focused on something specific to the school situation; the child can leave the parents or other attachment figures to go somewhere other than school. In treating separation anxiety in children, parents are often included to help structure the exercises and also to address parental reaction to childhood anxiety. Social Anxiety Disorder (Social Phobia) SAD is more than exaggerated shyness. Individuals with just performance anxiety, which is a subtype of SAD, usually have no difficulty with social interaction, but when they must do something specific in front of people, anxiety takes over and they focus on the possibility that they will embarrass themselves. The most common type of performance anxiety, to which most people can relate, is public speaking. Other situations that commonly provoke performance anxiety are eating in a restaurant or signing a paper or check in front of a person or people who are watching. Anxiety-provoking physical reactions include blushing, sweating, trembling, or, for males, urinating in a public restroom (“bashful bladder” or paruresis). Statistics In a given 1-year period, the prevalence is 6.8%, and 8.2% in adolescents. This makes SAD second only to specific phobia as the most prevalent anxiety disorder, afflicting more than 35 million people in the United States alone, based on current population estimates. Unlike other anxiety disorders for which females predominate, the sex ratio for SAD is nearly 50:50. SAD usually begins during adolescence, with a peak age of onset around 13 years. SAD also tends to be more prevalent in people who are young (18–29 years), undereducated, single, and of low socioeconomic class. Causes Mogg and colleagues showed that socially anxious individuals more quickly recognized angry faces than “normals”, whereas “normals” remembered the accepting expressions. Why should we inherit a tendency to fear angry faces? Our ancestors probably avoided hostile, angry, domineering people who might attack or kill them. Jerome Kagan and his colleagues have demonstrated that some infants are born with a temperamental profile or trait of inhibition or shyness that is evident as early as 4 months of age. Four-month-old infants with this trait become more agitated and cry more frequently when presented with toys or other age-appropriate stimuli than infants without the trait. Treatment Clark and colleagues evaluated a cognitive therapy program that emphasized real-life experiences during therapy to disprove automatic perceptions of danger. This is a superior treatment. Subsequent studies indicated that this treatment was clearly superior to a second very credible treatment, interpersonal psychotherapy (IPT) both immediately after treatment and at a 1-year follow-up, even when delivered in a center specializing in treatment with IPT. Results of numerous studies suggest that severely socially anxious adolescents can attain relatively normal functioning in school and other social settings after receiving cognitive behavioral treatment. Since 1999, the SSRIs Paxil, Zoloft, and Effexor have received approval from the Food and Drug Administration for treatment of SAD based on studies showing effectiveness compared with placebo. One impressive study compared Clark’s cognitive therapy described earlier with the SSRI drug Prozac, along with instructions to the patients with SAD to attempt to engage in more social situations (self-exposure). Both treatments did well, but the psychological treatment was substantially better at all times, with most patients cured or nearly cured with few remaining symptoms. Several exciting studies suggest that adding the drug D-cycloserine (DCS) to cognitive-behavioral treatments significantly enhances the effects of treatment. This drug works in the amygdala, a structure in the brain involved in the learning and unlearning of fear and anxiety. Unlike SSRIs, this drug is known to facilitate extinction of anxiety by modifying neurotransmitter flow in the glutamate system. Selective Mutism Now grouped with the anxiety disorders in DSM-5, selective mutism (SM) is a rare childhood disorder characterized by a lack of speech in one or more settings in which speaking is socially expected. In fact, speech in selective mutism commonly occurs in some settings, such as home, but not others, such as school, hence the term “selective”. In order to meet diagnostic criteria for SM, the lack of speech must occur for more than one month and cannot be limited to the first month of school. Trauma-and Stressor-Related Disorders DSM-5 consolidates a group of formerly disparate disorders that all develop after a relatively stressful life event, often an extremely stressful or traumatic life event. This set of disorders—trauma and stressor-related disorders—include attachment disorders in childhood following inadequate or abusive childrearing practices, adjustment disorders characterized by persistent anxiety and depression following a stressful life event, and reactions to trauma such as posttraumatic stress disorder and acute stress disorder. Posttraumatic Stress Disorder (PTSD) DSM-5 describes the setting event for PTSD as exposure to a traumatic event during which an individual experiences or witnesses death or threatened death, actual or threatened serious injury, or actual or threatened sexual violation. Victims reexperience the event through memories and nightmares. When memories occur suddenly, accompanied by strong emotion, and the victims find themselves reliving the event, they are having a flashback. Victims most often avoid anything that reminds them of the trauma. They are sometimes unable to remember certain aspects of the event. It is possible that victims unconsciously attempt to avoid the experience of emotion itself, like people with panic disorder, because intense emotions could bring back memories of the trauma. Victims typically are chronically overaroused, easily startled, and quick to anger. New to DSM-5 is the addition of “reckless or self-destructive behavior” under the PTSD E criteria as one sign of increased arousal and reactivity. Also new to DSM-5 is the addition of a “dissociative” subtype describing victims who do not necessarily react with the reexperiencing or hyperarousal, characteristic of PTSD. Since many individuals experience strong reactions to stressful events that typically disappear within a month, the diagnosis of PTSD cannot be made until at least one month after the occurrence of the traumatic event. In PTSD with delayed onset, individuals show few or no symptoms immediately or for months after a trauma, but at least 6 months later, and perhaps years afterward develop full-blown PTSD. As we noted, PTSD cannot be diagnosed until a month after the trauma. In DSM-IV a disorder called acute stress disorder was introduced. This is really PTSD, or something very much like it, occurring within the first month after the trauma, but the different name emphasizes the severe reaction that some people have immediately. Statistics In the population as a whole, surveys indicate that 6.8% have experienced PTSD at some point in their life. The highest rates are associated with experiences of rape; being held captive, tortured, or kidnapped; or being badly assaulted. What accounts for the discrepancies between the low rate of PTSD in citizens who endured bombing and shelling in London and Beirut and the relatively high rate in victims of assaultive violence? Close exposure to the trauma seems to be necessary to developing this disorder. Since a diagnosis of PTSD predicts suicidal attempts independently of any other problem, such as alcohol abuse, every case should be taken very seriously. Causes We know that intensity of exposure to assaultive violence contributes to the etiology of PTSD, but does not account for all of it. A family history of anxiety suggests a generalized biological vulnerability for PTSD. Nevertheless, as with other disorders, there is little or no evidence that genes directly cause PTSD. While all experienced the same traumatic experience, specific characteristics of what is referred to as the serotonin transporter gene involving two short alleles (SS) described as increasing the probability of becoming depressed. Breslau, Davis, and Andreski demonstrated among a random sample of 1,200 individuals that characteristics such as a tendency to be anxious, as well as factors such as minimal education, predict exposure to traumatic events in the first place and therefore an increased risk for PTSD. Family instability is one factor that may instill a sense that the world is an uncontrollable, potentially dangerous place. The results from a number of studies are consistent in showing that, if you have a strong and supportive group of people around you, it is much less likely you will develop PTSD after a trauma. Positive coping strategies involving active problem solving seemed to be protective, whereas becoming angry and placing blame on others were associated with higher levels of PTSD. A number of studies show that support from loved ones reduces cortisol secretion and hypothalamic–pituitary–adrenocortical (HPA) axis activity in children during stress. It seems clear that PTSD involves a number of neurobiological systems, particularly elevated or restricted corticotropin-releasing factor (CRF), which indicates heightened activity in the HPA axis. Treatment In psychoanalytic therapy, reliving emotional trauma to relieve emotional suffering is called catharsis. Unlike the object of a specific phobia, a traumatic event is difficult to recreate, and few therapists want to try. Therefore, imaginal exposure, in which the content of the trauma and the emotions associated with it are worked through systematically, has been used for decades under a variety of names. At present, the most common strategy to achieve this purpose with adolescents or adults is to work with the victim to develop a narrative of the traumatic experience that is then reviewed extensively in therapy. Cognitive therapy to correct negative assumptions about the trauma—such as blaming oneself in some way, feeling guilty, or both—is often part of treatment. Some of the drugs, such as SSRIs (e.g., Prozac and Paxil), that are effective for anxiety disorders in general have been shown to be helpful for PTSD, perhaps because they relieve the severe anxiety and panic attacks so prominent in this disorder. Adjustment disorders Adjustment disorders describe anxious or depressive reactions to life stress that are generally milder than one would see in acute stress disorder or PTSD but are nevertheless impairing in terms of interfering with work or school performance, interpersonal relationships, or other areas of living. The stressful events themselves would not be considered traumatic but it is clear that the individual is nevertheless unable to cope with the demands of the situation and some intervention is typically required. If the symptoms persist for more than six months after the removal of the stress or its consequences, the adjustment disorder would be considered “chronic”. Attachment disorders Attachment disorders refers to disturbed and developmentally inappropriate behaviors in children, emerging before five years of age, in which the child is unable or unwilling to form normal attachment relationships with caregiving adults. These seriously maladaptive patterns are due to inadequate or abusive child-rearing practices. In either case the result is a failure to meet the child’s basic emotional needs for affection, comfort, or even providing for the basic necessities of daily living. ❖ In reactive attachment disorder the child will support, and nurturance and will seldom respond to offers from caregivers to provide this kind of care. ⮚ Generally they would evidence lack of responsiveness, limited positive affect, and additional heightened emotionality, such as fearfulness and intense sadness. ❖ In disinhibited social engagement disorder, a similar set of child rearing circumstances— perhaps including early persistent harsh punishment—would result in a pattern of behavior in which the child shows no inhibitions whatsoever to approaching adults. ⮚ Such a child might engage in inappropriately intimate behavior by showing a willingness to immediately accompany an unfamiliar adult figure somewhere without first checking back with a caregiver. Obsessive-Compulsive and Related Disorders Obsessive-Compulsive Disorder In other anxiety disorders, the danger is usually in an external object or situation, or at least in the memory of one. In OCD, the dangerous event is a thought, image, or impulse that the client attempts to avoid as completely as someone with a snake phobia avoids snakes. Obsessions are intrusive and mostly nonsensical thoughts, images, or urges that the individual tries to resist or eliminate. Compulsions are the thoughts or actions used to suppress the obsessions and provide relief. Based on statistically associated groupings, there are four major types of obsessions and each is associated with a pattern of compulsive behavior. symmetry obsessions account for most obsessions (26.7%) “forbidden thoughts or actions” (21%) cleaning and contamination (15.9%) and hoarding (15.4%) Symmetry refers to keeping things in perfect order or doing something in a specific way. Obsessions with symmetry lead to ordering and arranging or repeating rituals. People with aggressive (forbidden) obsessive impulses may feel they are about to yell out a swear word in church. Forbidden thoughts or actions seem to lead to checking rituals. Checking rituals serve to prevent an imagined disaster or catastrophe. Many are logical, such as repeatedly checking the stove to see whether you turned it off, but severe cases can be illogical. For example, Richard thought that if he did not eat in a certain way he might become possessed. A mental act, such as counting, can also be a compulsion. Obsessions with contamination lead to washing rituals that may restore a sense of safety and control. ❖ It is also common for tic disorder, characterized by for example), to co-occur in patients with OCD (particularly children) or in their families. ⮚ More complex tics with involuntary vocalizations are referred to as Tourette’s disorder. ⮚ In some cases, these movements are not tics but may be compulsions, as they were in the case of Frank in Chapter 3 who kept jerking his leg if thoughts of seizures entered his head. ⮚ The obsessions in tic-related OCD are almost always related to symmetry. Statistics OCD has a ratio of female to male that is nearly 1:1. Age of onset ranges from childhood through the 30s, with a median age of onset of 19. The age of onset peaks earlier in males (13 to 15) than in females (20 to 24). Causes When clients with OCD equate thoughts with the specific actions or activity represented by the thoughts, this is called thought–action fusion. Thought–action fusion may, in turn, be caused by attitudes of excessive responsibility and resulting guilt developed during childhood, when even a bad thought is associated with evil intent. Treatment The most effective seem to be those that specifically inhibit the reuptake of serotonin, such as clomipramine or the SSRIs, which benefit up to 60% of patients with OCD, with no particular advantage to one drug over another. The most effective approach is called exposure and ritual prevention (ERP), a process whereby the rituals are actively prevented and the patient is systematically and gradually exposed to the feared thoughts or situations. More recent innovations to evidence-based psychological treatments for OCD have examined the efficacy of cognitive treatments with a focus on the overestimation of threat, the importance and control of intrusive thoughts, the sense of inflated responsibility present in patients with OCD who think they alone may be responsible for preventing a catastrophe, as well as the need for perfectionism and certainty present in these patients. ERP, with or without the drug, produced superior results to the drug alone, with 86% responding to ERP alone versus 48% to the drug alone. Combining the treatments did not produce any additional advantage. Psychosurgery is one of the more radical treatments for OCD. “Psychosurgery” is a misnomer that refers to neurosurgery for a psychological disorder. Jenike and colleagues reviewed the records of 33 patients with OCD, most of them extremely severe cases who had failed to respond to either drug or psychological treatment. After a specific surgical lesion to the cingulate bundle (cingulotomy), approximately 30% benefited substantially. Body Dysmorphic Disorder Most people fantasize about improving something, but some relatively normal-looking people think they are so ugly they refuse to interact with others or otherwise function normally for fear that people will laugh at their ugliness. This curious affliction is called body dysmorphic disorder (BDD), and at its center is a preoccupation with some imagined defect in appearance by someone who actually looks reasonably normal. The disorder has been referred to as “imagined ugliness”. For many years, BDD was considered a somatoform disorder because its central feature is a psychological preoccupation with somatic (physical) issues. But increasing evidence indicated it was more closely related to OCD, accounting for its relocation to the obsessive-compulsive and related disorders section in DSM-5. People with BDD complain of persistent, intrusive, and horrible thoughts about their appearance, and they engage in such compulsive behaviors as repeatedly looking in mirrors to check their physical features. Quite understandably, suicidal ideation, suicide attempts, and suicide itself are typical consequences of this disorder. The prevalence of BDD is hard to estimate because by its very nature it tends to be kept secret. In mental health clinics, the disorder is also uncommon because most people with BDD seek other types of health professionals, such as plastic surgeons and dermatologists. BDD is seen equally in men and women. Men tend to focus on body build, genitals, and thinning hair and tend to have more severe BDD. Women focus on more varied body areas and are more likely to also have an eating disorder. Age of onset ranges from early adolescence through the 20s, peaking at the age of 16–17. One study of 62 consecutive outpatients with BDD found that the degree of psychological stress, quality of life, and impairment were generally worse than comparable indices in patients with depression, diabetes, or a recent myocardial infarction (heart attack) on several questionnaire measures. Perhaps more significantly, there are two, and only two, treatments for BDD with any evidence of effectiveness, and these treatments are the same found effective in OCD. First, drugs that block the re-uptake of serotonin, such as clomipramine (Anafranil) and fluvoxamine (Luvox), provide relief to at least some people. A second controlled study reported similar findings for fluoxetine (Prozac), with 53% showing a good response compared with 18% on placebo after 3 months. Exposure and response prevention, the type of cognitive-behavioral therapy effective with OCD, has also been successful with BDD. As with OCD, cognitive-behavioral therapy tends to produce better and longer lasting outcomes compared to medication alone. Other Obsessive-Compulsive and Related Disorders Hoarding Disorder The three major characteristics of this problem are excessive acquisition of things, difficulty discarding anything, and living with excessive clutter under conditions best characterized as gross disorganization. Basically, these individuals usually begin acquiring things during their teenage years and often experience great pleasure, even euphoria, from shopping or otherwise collecting various items. These individuals then experience strong anxiety and distress about throwing anything away, because everything has either some potential use or sentimental value in their minds, or simply becomes an extension of their own identity. The average age when these people come for treatment is approximately 50, after many years of hoarding. Cognitive and emotional abnormalities associated with hoarding alluded to above include extraordinarily strong emotional attachment to possessions, an exaggerated desire for control over possessions, and marked deficits in deciding when a possession is worth keeping or not (all possessions are believed to be equally valuable). People who hoard animals comprise a special group that is now being investigated more closely. Animal hoarders are characterized by the failure or inability to care for the animals or provide suitable living quarters, which results in threats to health and safety due to unsanitary conditions associated with accumulated animal waste. The hoarding group was characterized by attribution of human characteristics to their animals, the presence of more dysfunctional current relationships (with other people) and significantly greater mental health concerns. Trichotillomania (Hair Pulling Disorder) and Excoriation (Skin Picking Disorder) Trichotillomania The urge to pull out one’s own hair from anywhere on the body, including the scalp, eyebrows, and arms, is referred to as trichotillomania. This behavior results in noticeable hair loss, distress, and significant social impairments. Compulsive hair pulling is more common than once believed and is observed in between 1% and 5% of college students, with females reporting the problem more than males. There may be some genetic influence on trichotillomania, with one study finding a unique genetic mutation in a small number of people. Excoriation (skin picking disorder) is characterized, as the label implies, by repetitive and compulsive picking of the skin, leading to tissue damage. There can be significant embarrassment, distress, and impairment in terms of social and work functioning. Excoriation is also largely a female disorder. Prior to DSM-5, both disorders were classified under impulse control disorders, but it has been established that these disorders often co-occur with obsessive-compulsive disorder and body dysmorphic disorder, as well as with each other. Until recently it was assumed that the repetitive behaviors of hair pulling and skin picking function to relieve stress or tension. While this seems to be the case for many patients, a substantial number of individuals do not engage in this behavior to relieve tension and do not evidence tension relief. For this reason diagnostic criteria referring to tension relief, present in DSM-IV, have been removed in DSM-5. Psychological treatments, particularly an approach called “habit reversal training”, has the most evidence for success with these two disorders. In this treatment, patients are carefully taught to be more aware of their repetitive behavior, particularly as it is just about to begin, and to then substitute a different behavior, such as chewing gum, applying a soothing lotion to the skin, or some other reasonably pleasurable but harmless behavior. Drug treatments, mostly serotonin-specific reuptake inhibitors, hold some promise, particularly for trichotillomania, but the results have been mixed with excoriation. Somatic Symptom and Related Disorders and Dissociative Disorders Somatic Symptom Disorder For many years, this disorder was called Briquet’s syndrome, but symptom disorder. People with somatic symptom disorder do not always feel the urgency to take action but continually feel weak and ill, and they avoid exercising, thinking it will make them worse. Another common example of a somatic symptom disorder would be the experience of severe pain in which psychological factors play a major role in maintaining or exacerbating the pain whether there is a clear physical reason for the pain or not. Illness Anxiety Disorder Illness anxiety disorder was formerly known as “hypochondriasis”, which is still the term widely used among the public. In illness anxiety disorder as we know it today, physical symptoms are either not experienced at the present time or are very mild, but severe anxiety is focused on the possibility of having or developing a serious disease. If one or more physical symptoms are relatively severe and are associated with anxiety and distress the diagnosis would be somatic symptom disorder. In illness anxiety disorder the concern is primarily with the idea of being sick instead of the physical symptom itself. Anxiety and mood disorders are often comorbid with somatic symptom disorders; that is, if individuals with somatic symptom disorders have additional diagnoses, these most likely are anxiety or mood disorders. Somatic symptom disorder and illness anxiety disorder are characterized by anxiety or fear that one has a serious disease. Because a key feature of this disorder is preoccupation with physical symptoms, individuals with these disorders almost always go initially to family physicians. Many of these individuals mistakenly believe they have a disease, a difficult-to-shake belief sometimes referred to as “disease conviction”. Therefore, along with anxiety focused on the possibility of disease or illness, disease conviction is a core feature of both disorders. Although all disorders include characteristic concern with physical symptoms, patients with panic disorder typically fear immediate symptom-related catastrophes that may occur during the few minutes they are having a panic attack, and these concerns lessen between attacks. Individuals with somatic symptom disorders, on the other hand, focus on a longterm process of illness and disease (for example, cancer or AIDS). Statistics The prevalence of DSM-IV hypochondriasis, which would encompass illness anxiety disorder and part of somatic symptom disorder, has been estimated to be from 1% to 5%. It was thought for a long time that somatic symptom disorders were more prevalent in elderly populations, but this does not seem to be true. The proportion of all those seeing a doctor with these disorders is about the same. Linda’s disorder developed during adolescence, which is the typical age of onset. A number of studies have demonstrated that individuals with what would now be somatic symptom disorder tend to be women, unmarried, and from lower socioeconomic groups. Obviously, individuals with somatic symptom disorders overuse and misuse the health-care system, with medical bills as much as 9 times more than the average patient. As with anxiety disorders, culture-specific syndromes seem to fit comfortably with somatic symptom disorders. Among these is the disorder of koro, in which there is the belief, accompanied by severe anxiety and sometimes panic, that the genitals are retracting into the abdomen. Why does koro occur in Chinese cultures? Rubin points to the central importance of sexual functioning among Chinese males. He notes that typical sufferers are guilty about excessive masturbation, unsatisfactory intercourse, or promiscuity. These kinds of events may predispose men to focus their attention on their sexual organs, which could exacerbate anxiety and emotional arousal, much as it does in the anxiety disorders. Another culture-specific disorder, prevalent in India, is an anxious concern about losing semen, something that obviously occurs during sexual activity. The disorder, called dhat, is associated with a vague mix of physical symptoms, including dizziness, weakness, and fatigue. These low-grade depressive or anxious symptoms are simply attributed to a physical factor, semen loss. When the problem is severe enough to meet criteria for disorder, the sex ratio is approximately 2:1 female to male. Causes Faulty interpretation of physical signs and sensations as evidence of physical illness is central, so almost everyone agrees that these disorders are basically disorders of cognition or perception with strong emotional contributions. Using procedures from cognitive science such as the Stroop test, a number of investigators have confirmed that participants with these disorders show enhanced perceptual sensitivity to illness cues. Smeets, de Jong, and Mayer demonstrated that individuals with these disorders, compared with “normals,” take a “better safe than sorry” approach to dealing with even minor physical symptoms by getting them checked out as soon as possible. It is therefore quite possible, as in panic disorder, that individuals who develop somatic symptom disorder or illness anxiety disorder have learned from family members to focus their anxiety on specific physical conditions and illness. The “benefits” of being sick might contribute to the development of the disorder in some people. A “sick person” who receives increased attention for being ill and is able to avoid work or other responsibilities is described as adopting a “sick role.” In its severe form, a somewhat startling finding emerges from studies of somatic symptom disorder. This disorder is strongly linked in family and genetic studies to antisocial personality disorder (ASPD), which is characterized by vandalism, persistent lying, theft, irresponsibility with finances and at work, and outright physical aggression. Individuals with ASPD seem insensitive to signals of punishment and to the negative consequences of their often impulsive behavior, and they apparently experience little anxiety or guilt. Treatment Surprisingly, clinical reports indicate that reassurance and education seems to be effective in some cases “surprisingly” because, by definition, patients with these disorders are not supposed to benefit from reassurance about their health. Taking the time to explain in some detail the nature of the patient’s disorder (explanatory therapy) in an educational framework was associated with a significant reduction in fears and beliefs about somatic symptoms and a decrease in health-care usage, and these gains were maintained at the follow-up. CBT focused on identifying and challenging illness-related misinterpretations of physical sensations and on showing patients how to create “symptoms” by focusing attention on certain body areas. Bringing on their own symptoms persuaded many patients that such events were under their control. Not surprisingly, these same types of drugs (antidepressants) are useful for anxiety and depression. In one study, CBT and the drug paroxetine (Paxil), a selective-serotonin reuptake inhibitor (SSRI), were both effective, but only CBT was significantly different from a placebo condition. A related somatic symptom disorder is called psychological factors affecting medical condition. The essential feature of this disorder is the presence of a diagnosed medical condition such as asthma, diabetes, or severe pain clearly caused by a known medical condition such as cancer that is adversely affected (increased in frequency or severity) by one or more psychological or behavioral factors. Conversion Disorder (Functional Neurological Symptom Disorder) The term conversion has been used off and on since the Middle Ages but was popularized by Freud, who believed the anxiety resulting from unconscious conflicts somehow was “converted” into physical symptoms to find expression. In DSM-5, “functional neurological symptom disorder” is a subtitle to conversion disorder because the term is more often used by neurologists who see the majority of patients receiving a conversion disorder diagnosis, and because the term is more acceptable to patients. “Functional” refers to a symptom without an organic cause. Conversion disorders generally have to do with physical malfunctioning, such as paralysis, blindness, or difficulty speaking (aphonia), without any physical or organic pathology to account for the malfunction. Most conversion symptoms suggest that some kind of neurological disease is affecting sensory–motor systems, although conversion symptoms can mimic the full range of physical malfunctioning. In addition to blindness, paralysis, and difficulty speaking (aphonia), conversion symptoms may include total mutism and the loss of the sense of touch. Although she was not paralyzed, her specific symptoms included weakness in her legs and difficulty keeping her balance, with the result that she fell often. This particular type of conversion symptom is called astasia-abasia. Another relatively common symptom is globus hystericus, the sensation of a lump in the throat that makes it difficult to swallow, eat, or sometimes talk. It was long thought that patients with conversion reactions had the same quality of indifference to the symptoms thought to be present in some people with severe somatic symptom disorder. This attitude, referred to as la belle indifférence, was considered a hallmark of conversion reactions, but, unfortunately, this turns out not to be the case. Conversion symptoms often seem to be precipitated by marked stress. Often this stress takes the form of a physical injury. It is possible that at least some people who experience miraculous cures during religious ceremonies may have been suffering from conversion reactions. Individuals with the conversion symptom of blindness can usually avoid objects in their visual field, but they will tell you they can’t see the objects. Similarly, individuals with conversion symptoms of paralysis of the legs might suddenly get up and run in an emergency and then be astounded they were able to do this. The investigators found that the conversion tremor, as compared with the voluntary tremor, was associated with lower activity in the right inferior parietal cortex. Interestingly, this is an area of the brain that functions to compare internal predictions with actual events. In other words, if an individual wants to move her arm and then she decides to go ahead and move it, this area of the brain determines if the desired action has occurred. Malingerers are fully aware of what they are doing and are clearly attempting to manipulate others to gain a desired end. It can also be difficult to distinguish between individuals who are truly experiencing conversion symptoms in a seemingly involuntary way and malingerers who are good at faking symptoms. They are either trying to get out of something, such as work or legal difficulties, or they are attempting to gain something, such as a financial settlement. More puzzling is a set of conditions called factitious disorders, which fall somewhere between malingering and conversion disorders. The symptoms are under voluntary control, as with malingering, but there is no obvious reason for voluntarily producing the symptoms except, possibly, to assume the sick role and receive increased attention. When an individual deliberately makes someone else sick, the condition is called factitious disorder imposed on another. It was also known previously as Munchausen syndrome by proxy. In any case, it is really an atypical form of child abuse. Statistics Conversion disorders are relatively rare in mental health settings, but remember that people who seek help for this condition are more likely to consult neurologists or other specialists. The prevalence estimate in neurological settings is high, averaging about 30%. Like severe somatic symptom disorder, conversion disorders are found primarily in women and typically develop during adolescence or slightly thereafter. If the patients believed the diagnosis of conversion disorder when it was given to them, and otherwise perceived themselves as being in good health and functioning well at work and at home, they had a better chance of recovering from their psychologically based seizures. Causes Freud described four basic processes in the development of conversion disorder. First, the individual experiences a traumatic event—in Freud’s view, an unacceptable, unconscious conflict. Second, because the conflict and the resulting anxiety are unacceptable, the person represses the conflict, making it unconscious. Third, the anxiety continues to increase and threatens to emerge into consciousness, and the person “converts” it into physical symptoms, thereby relieving the pressure of having to deal directly with the conflict. ✧ This reduction of anxiety is considered to be the primary gain or reinforcing event that maintains the conversion. Fourth, the individual receives greatly increased attention and sympathy from loved ones and may also be allowed to avoid a difficult situation or task. ✧ Freud considered such attention or avoidance to be the secondary gain, the secondarily reinforcing set of events. Adolescents with the conversion disorder were more likely to have experienced some significant stress and adjustment difficulties, such as substantial school difficulties, or the loss of a significant figure in their lives, and they rated their mothers as overinvolved and overprotective on a rating scale. Stone and colleagues in the study described earlier on “indifference” to conversion symptoms found no difference in distress over symptoms among patients with conversion disorder compared with patients with organic disease. Social and cultural influences also contribute to conversion disorder, which, like somatic symptom disorder, tends to occur in less educated, lower socioeconomic groups where knowledge about disease and medical illness is not well developed. Treatment As in the case of Anna O., therapeutic assistance in reexperiencing or “reliving” the event (catharsis) is a reasonable first step. The therapist must also work hard to reduce any reinforcing or supportive consequences of the conversion symptoms (secondary gain). Dissociative Disorders Depersonalization-Derealization Disorder During an episode of depersonalization, your perception alters so that you temporarily lose the sense of your own reality, as if you were in a dream and you were watching yourself. During an episode of derealization, your sense of the reality of the external world is lost. When feelings of unreality are so severe and frightening that they dominate an individual’s life and prevent normal functioning, clinicians may diagnose the rare depersonalization-derealization disorder. Mean age of onset was 16 years, and the course tended to be chronic. Although both groups were of equal intelligence, the participants with depersonalization disorder showed a distinct cognitive profile, reflecting some specific cognitive deficits on measures of attention, processing of information, short-term memory, and spatial reasoning. Patients with depersonalization disorder showed greatly reduced emotional responding compared with other groups, reflecting a tendency to selectively inhibit emotional expression. Other studies note dysregulation in the hypothalamic–pituitary–adrenocortical (HPA) axis among these patients, compared with normal controls. Dissociative Amnesia People who are unable to remember anything, including who they are, are said to suffer from generalized amnesia. Generalized amnesia may be lifelong or may extend from a period in the more recent past, such as 6 months or a year previously. Far more common than general amnesia is localized or selective amnesia, a failure to recall specific events, usually traumatic, that occur during a specific period. In most cases of dissociative amnesia, the forgetting is selective for traumatic events or memories rather than generalized. A subtype of dissociative amnesia is referred to as dissociative fugue with fugue literally meaning “flight” (fugitive is from the same root). In these curious cases, memory loss revolves around a specific incident—an unexpected trip (or trips). Mostly, individuals just take off and later find themselves in a new place, unable to remember why or how they got there. During these trips, a person sometimes assumes a new identity or at least becomes confused about the old identity. Dissociative amnesia seldom appears before adolescence and usually occurs in adulthood. Once dissociative disorders do appear, however, they may continue well into old age. Estimates of prevalence range anywhere from 1.8% to 7.3%, suggesting that dissociative amnesia is the most prevalent of all the dissociative disorders. An apparently distinct dissociative state not found in Western cultures is called amok (as in “running amok”). Most people with this disorder are males. Amok has attracted attention because individuals in this trancelike state often brutally assault and sometimes kill people or animals. Dissociative disorders differ in important ways across cultures. In many areas of the world, dissociative phenomena may occur as a trance or possession. Dissociative Identity Disorder People with dissociative identity disorder (DID) may adopt as many as 100 new identities, all simultaneously coexisting, although the average number is closer to 15. In some cases, the identities are complete, each with its own behavior, tone of voice, and physical gestures. But in many cases, only a few characteristics are distinct, because the identities are only partially independent, so it is not true that there are “multiple” complete personalities. Therefore, the name of the disorder was changed in the last edition of the DSM, DSM-IV, from multiple personality disorder to DID. Alters is the shorthand term for the different identities or personalities in DID. The person who becomes the patient and asks for treatment is usually a “host” identity. The transition from one personality to another is called a switch. Usually, the switch is instantaneous (although in movies and on television it is often drawn out for dramatic effect). Physical transformations may occur during switches. Posture, facial expressions, patterns of facial wrinkling, and even physical disabilities may emerge. In one study, changes in handedness occurred in 37% of the cases. Objective assessment of memory, particularly implicit (unconscious) memory, reveals that the memory processes in patients with DID do not differ from “normals” when the methodologies of cognitive science are used. This is in contrast to reports from interviews with patients with DID that suggest that memories are different from one alter to the next. These findings on faking and the effect of hypnosis led Spanos to suggest that the symptoms of DID could mostly be accounted for by therapists who inadvertently suggested the existence of alters to suggestible individuals, a model known as the “sociocognitive model” because the possibility of identity fragments and early trauma is socially reinforced by a therapist. These optical differences have been confirmed by S. D. Miller, who demonstrated that DID patients had 4.5 times the average number of changes in optical functioning in their alter identities than control patients who simulated alter personalities. ⮚ Miller concludes that optical changes, including measures of visual acuity, manifest refraction, and eye muscle balance, would be difficult to fake. Using functional magnetic resonance imaging (fMRI) procedures, changes in brain function were observed in one patient while switching from one personality to another. Specifically, this patient showed changes in hippocampal and medial temporal activity after the switch. Statistics Jonah had 4 identities, and Anna O. only 2, but the average number of alter personalities is reported by clinicians as closer to 15. Of people with DID, the ratio of females to males is as high as 9:1, although these data are based on accumulated case studies rather than survey research. The onset is almost always in childhood, often as young as 4 years of age, although it is usually approximately 7 years after the appearance of symptoms before the disorder is identified. The form DID takes does not seem to vary substantially over the person’s lifespan, although some evidence indicates the frequency of switching decreases with age. A large percentage of DID patients have simultaneous psychological disorders that may include anxiety, substance abuse, depression, and personality disorders. Some investigators believe that most of DID symptoms can be best accounted for by characteristics of borderline personality disorder. Because auditory hallucinations are common, DID is often misdiagnosed as a psychotic disorder. But the voices in DID are reported by patients as coming from inside their heads, not outside as in psychotic disorders. Causes Almost every patient presenting with this disorder reports to their mental health professional being horribly, often unspeakably, abused as a child. Imagine you are a child in a situation like this. What can you do? You’re too young to run away. You’re too young to call the authorities. Although the pain may be unbearable, you have no way of knowing it is unusual or wrong. But you can do one thing. You can escape into a fantasy world; you can be somebody else. Putnam and colleagues examined 100 cases and found that 97% of the patients had experienced significant trauma, usually sexual or physical abuse. Sixty-eight percent reported incest. Some children reported being buried alive. Some were tortured with matches, steam irons, razor blades, or glass. A study of 428 adolescent twins demonstrated that a surprisingly major portion of the cause of dissociative experience could be attributed to a chaotic, nonsupportive family environment. Some evidence also shows that the “developmental window” of vulnerability to the abuse that leads to DID closes at approximately 9 years of age. After that, DID is unlikely to develop, although severe PTSD might. Suggestibility is a personality trait distributed normally across the population, much like weight and height. Some people are more suggestible than others; some are relatively immune to suggestibility; and the majority fall in the midrange. There is also the phenomenon of self-hypnosis, in which individuals can dissociate from most of the world around them and “suggest” to themselves that, for example, they won’t feel pain in one of their hands. According to the autohypnotic model, people who are suggestible may be able to use dissociation as a defense against extreme trauma. There is some evidence of smaller hippocampal and amygdala volume in patients with DID compared with “normals”. Strong evidence exists that sleep deprivation produces dissociative symptoms such as marked hallucinatory activity. In fact, the symptoms of individuals with DID seem to worsen when they feel tired. If early sexual abuse did occur but is not remembered because of dissociative amnesia, it is crucially important to reexperience aspects of the trauma under the direction of a skilled therapist to relieve current suffering. On the other hand, if memories of early trauma are inadvertently created in response to suggestions by a careless therapist but seem real to the patient, false accusations against loved ones could lead to irreversible family breakup and, perhaps, unjust prison sentences for those falsely accused as perpetrators. Treatment The episodes are so clearly related to current life stress that prevention of future episodes usually involves therapeutic resolution of the distressing situations and increasing the strength of personal coping mechanisms. When necessary, therapy focuses on recalling what happened during the amnesic or fugue states, often with the help of friends or family who know what happened, so that patients can confront the information and integrate it into their conscious experience. For more difficult cases, hypnosis or benzodiazepines (minor tranquilizers) have been used, with suggestions from the therapist that it is okay to remember the events. Hypnosis is often used to access unconscious memories and bring various alters into awareness. Because the process of dissociation may be similar to the process of hypnosis, the latter may be a particularly efficient way to access traumatic memories. Mood Disorders and Suicide The disorders described in this chapter used to be categorized under several general labels, such as “depressive disorders”, “affective disorders”, or even “depressive neuroses”. Beginning with the third edition of the Diagnostic and Statistical Manual (DSM-III), published by the American Psychiatric Association in 1980, these problems have been grouped under the heading mood disorders because they are characterized by gross deviations in mood. Major Depressive Episode The most commonly diagnosed and most severe depression is called a major depressive episode. The DSM-5 criteria describes it as an extremely depressed mood state that lasts at least 2 weeks and includes cognitive symptoms (such as feelings of worthlessness and indecisiveness) and disturbed physical functions (such as altered sleeping patterns, significant changes in appetite and weight, or a notable loss of energy) to the point that even the slightest activity or movement requires an overwhelming effort. The episode is typically accompanied by a general loss of interest in things and an inability to experience any pleasure from life, including interactions with family or friends or accomplishments at work or at school. Although all symptoms are important, evidence suggests that the most central indicators of a full major depressive episode are the physical changes (sometimes called somatic or vegetative symptoms). Anhedonia (loss of energy and inability to engage in pleasurable activities or have any “fun”) is more characteristic of these severe episodes of depression than are, for example, reports of sadness or distress. The duration of a major depressive episode, if untreated, is approximately 4 to 9 months. Manic Episode The second fundamental state in mood disorders is abnormally exaggerated elation, joy, or euphoria. In mania, individuals find extreme pleasure in every activity; some patients compare their daily experience of mania with a continuous sexual orgasm. They become extraordinarily active (hyperactive), require little sleep, and may develop grandiose plans, believing they can accomplish anything they desire. Speech is typically rapid and may become incoherent, because the individual is attempting to express so many exciting ideas at once; this feature is typically referred to as flight of ideas. DSM-5 criteria for a manic episode require a duration of only 1 week, less if the episode is severe enough to require hospitalization. Hospitalization could occur, for example, if the individual was engaging in a self-destructive buying spree, charging thousands of dollars in the expectation of making a million dollars the next day. Irritability is often part of a manic episode, usually near the end. The duration of an untreated manic episode is typically 3 to 4 months. DSM-5 also defines a hypomanic episode, a less severe version of a manic episode that does not cause marked impairment in social or occupational functioning and need last only 4 days rather than a full week. (Hypo means “below”; thus the episode is below the level of a manic episode.) Research suggests that manic episodes are characterized by dysphoric (anxious or depressive) features more commonly than was thought, and dysphoria can be severe. Individuals who experience either depression or mania are said to suffer from a unipolar mood disorder, because their mood remains at one “pole” of the usual depression-mania continuum. Someone who alternates between depression and mania is said to have a bipolar mood disorder traveling from one “pole” of the depression-elation continuum to the other and back again. An individual can experience manic symptoms but feel somewhat depressed or anxious at the same time; or be depressed with a few symptoms of mania. This episode is characterized as having “mixed features”. In fact, a strong body of evidence indicates that the two factors that most importantly describe mood disorders are severity and chronicity. Major Depressive Disorder The most easily recognized mood disorder is major depressive disorder, defined by the absence of manic, or hypomanic episodes before or during the disorder. If two or more major depressive episodes occurred and were separated by at least 2 months during which the individual was not depressed, the major depressive disorder is noted as being recurrent. Persistent Depressive Disorder (Dysthymia) Persistent Depressive Disorder shares many of the symptoms of major depressive disorder but differs in its course. There may be fewer symptoms (as few as 2, see DSM-5 Table 7.4) but depression remains relatively unchange over long periods, sometimes 20 or 30 years or more. Persistent depressive disorder (dysthymia) is defined as depressed mood that continues at least 2 years, during which the patient cannot be symptom free for more than 2 months at a time even though they may not experience all of the symptoms of a major depressive episode. This disorder differs from a major depressive disorder in the number of symptoms required, but mostly in the chronicity. It is considered more severe, since patients with persistent depression present with higher rates of comorbidity with other mental disorders, are less responsive to treatment, and show a slower rate of improvement over time. These individuals who suffer from both major depressive episodes and persistent depression with fewer symptoms are said to have double depression. In addition to rating severity of the episode as mild, moderate, or severe, clinicians use eight basic specifiers to describe depressive disorders. (1) with psychotic features (moodcongruent or mood-incongruent) (2) with anxious distress (mild to severe) (3) with mixed features (4) with melancholic features (5) with atypical features (6) with catatonic features (7) with peripartum onset, and (8) with seasonal pattern ❖ Psychotic features specifiers ⮚ Some individuals in the midst of a major depressive (or manic) episode may experience psychotic symptoms, specifically hallucinations (seeing or hearing things that aren’t there) and delusions (strongly held but inaccurate beliefs). ⮚ Patients may also have somatic (physical) delusions, believing, for example, that their bodies are rotting internally and deteriorating into nothingness. ⮚ Some may hear voices telling them how evil and sinful they are (auditory hallucinations). ✧ Such hallucinations and delusions are called mood congruent, because they seem directly related to the depression. ⮚ On rare occasions, depressed individuals might have other types of hallucinations or delusions such as delusions of grandeur (believing, for example, they are supernatural or supremely gifted) that do not seem consistent with the depressed mood. ✧ This is a mood-incongruent hallucination or delusion. ✧ Delusions of grandeur accompanying a manic episode are mood congruent. ⮚ Conditions in which psychotic symptoms accompany depressive episodes are relatively rare, occurring in 5% to 20% of identified cases of depression. ⮚ Psychotic features in general are associated with a poor response to treatment, greater impairment, and fewer weeks with minimal symptoms, compared with nonpsychotic depressed patients over a 10-year period. ❖ Anxious distress specifier ⮚ The presence and severity of accompanying anxiety, whether in the form of comorbid anxiety disorders (anxiety symptoms meeting the full criteria for an anxiety disorder) or anxiety symptoms that do not meet all the criteria for disorders. ⮚ For all depressive and bipolar disorders, the presence of anxiety indicates a more severe condition, makes suicidal thoughts and completed suicide more likely, and predicts a poorer outcome from treatment. ❖ Mixed features specifier ⮚ Predominantly depressive episodes that have several (at least three) symptoms of mania as described above would meet this specifier, which applies to major depressive episodes both within major depressive disorder and persistent depressive disorder. ❖ Melancholic features specifier ⮚ This specifier applies only if the full criteria for a major depressive episode have been met, whether in the context of a persistent depressive disorder or not. ⮚ Melancholic specifiers include some of the more severe somatic (physical) symptoms, such as early-morning awakenings, weight loss, loss of libido (sex drive), excessive or inappropriate guilt, and anhedonia (diminished interest or pleasure in activities). ❖ Catatonic features specifier ⮚ This serious condition involves an absence of movement (a stuporous state) or catalepsy, in which the muscles are waxy and semirigid, so a patient’s arms or legs remain in any position in which they are placed. ⮚ Catatonic symptoms may also involve excessive but random or purposeless movement. ❖ Atypical features specifier ⮚ While most people with depression sleep less and lose their appetite, individuals with this specifier consistently oversleep and overeat during their depression and therefore gain weight, leading to a higher incidence of diabetes. ⮚ Although they also have considerable anxiety, they can react with interest or pleasure to some things, unlike most depressed individuals. ⮚ The atypical group also has more symptoms, more severe symptoms, more suicide attempts, and higher rate of comorbid disorders including alcohol abuse. ❖ Peripartum onset specifier ⮚ Peri means “surrounding”, in this case the period of time just before and just after the birth. ⮚ Typically a somewhat higher incidence of depression is found postpartum (after the birth) than during the period of pregnancy itself. ⮚ In another recent important study, 14% of 10,000 women who gave birth screened positively for depression and fully 19.3% of those depressed new mothers had serious thoughts of harming themselves. ⮚ During the peripartum period (pregnancy and the 6 month period immediately following childbirth), early recognition of possible psychotic depressive (or manic) episodes is important, because in a few tragic cases a mother in the midst of an episode has killed her newborn child. ⮚ More minor reactions in adjustment to childbirth— called the “baby blues”—typically last a few days and occur in 40% to 80% of women between 1 and 5 days after delivery. ⮚ In peripartum depression, most people, including the new mother herself, have difficulty understanding why she is depressed, because they assume this is a joyous time. ❖ Seasonal pattern specifier ⮚ This temporal specifier applies to recurrent major depressive disorder (and also to bipolar disorders). ⮚ It accompanies episodes that occur during certain seasons (for example, winter depression). ⮚ (In bipolar disorder, individuals may become depressed during the winter and manic during the summer.) These episodes must have occurred for at least two years with no evidence of nonseasonal major depressive episodes occurring during that period of time. This condition is called seasonal affective disorder (SAD). ✧ Emerging evidence suggests that SAD may be related to daily and seasonal changes in the production of melatonin, a hormone secreted by the pineal gland. ✧ Light therapy is a promising treatment for seasonal affective disorder, often providing relief from depressive symptoms in just a few days. ✧ In phototherapy, a current treatment, most patients are exposed to 2 hours of bright light (2,500 lux) immediately on awakening. If the light exposure is effective, the patient begins to notice a lifting of mood within 3 to 4 days and a remission of winter depression in 1 to 2 weeks. The mean age of onset for major depressive disorder is 30 years, based on a large (43,000) and representative sample of the population of the United States, but 10% of all people who develop major depression are 55 or older when they have their first episode. Kessler and colleagues compared four age groups and found that fully 25% of people 18 to 29 years had already experienced major depression, a rate far higher than the rate for older groups when they were that age. Rohde et al. also looked at the incidence of major depressive disorder and four age groups spanning a longer period of time. They found that in children ages 5 to 12, 5% had experienced major depressive disorder. The acute grief most of us would feel eventually evolves into what is called integrated grief, in which the finality of death and its consequences are acknowledged and the individual adjusts to the loss. When grief lasts beyond typical time, mental health professionals again become concerned. ⮚ After 6 months to a year or so, the chance of recovering from severe grief without treatment is considerably reduced, and for approximately 7% of bereaved individuals), a normal process becomes a disorder. ⮚ At this stage, suicidal thoughts increase substantially and focus mostly on joining the beloved deceased. Many of the psychological and social factors related to mood disorders in general, including a history of past depressive episodes, also predict the development of what is called the syndrome of complicated grief, although this reaction can develop without a preexisting depressed state. Premenstrual Dysphoric Disorder (PMDD) Basically clinicians identified a small group of women, from 2% to 5%, who suffered from severe and sometimes incapacitating emotional reactions during the premenstrual period. But strong objections to making this condition an official diagnosis were based on concerns that women who were experiencing a very normal monthly physiological cycle, as part of being female, would now be classified as having a disorder, which would be very stigmatizing. A combination of physical symptoms, severe mood swings and anxiety are associated with incapacitation during this period of time. Disruptive Mood Dysregulation Disorder But the most important observation is that these children show no evidence of periods of elevated mood (mania), which has been a requirement for a diagnosis of bipolar disorder. These cases also differ from more typical conduct or ADHD conditions as well, since it is the intense negative affect that seems to be driving the irritability and marked inability to regulate mood. In view of the distinctive features of this condition reviewed above, it seemed very important to better describe these children up to 12 years of age as suffering from a diagnosis termed disruptive mood dysregulation disorder rather than have them continue to be mistakenly diagnosed with bipolar disorder or perhaps conduct disorder. Bipolar Disorders The key identifying feature of bipolar disorders is the tendency of manic episodes to alternate with major depressive episodes in an unending roller-coaster ride from the peaks of elation to the depths of despair. Bipolar II disorder, in which major depressive episodes alternate with hypomanic episodes rather than full manic episodes. The criteria for bipolar I disorder are the same, except the individual experiences a full manic episode. As in the criteria set for major depressive disorder, for the manic episodes to be considered separate, there must be a symptom-free period of at least 2 months between them. There is one specifier that is unique to bipolar I and II disorders: rapid-cycling specifier. Some people move quickly in and out of depressive or manic episodes. An individual with bipolar disorder who experiences at least four manic or depressive episodes within a year is considered to have a rapid-cycling pattern, which appears to be a severe variety of bipolar disorder that does not respond well to standard treatments. ⮚ In most cases, rapid cycling tends to increase in frequency over time and can reach severe states in which patients cycle between mania and depression without any break. ⮚ When this direct transition from one mood state to another happens, it is referred to as rapid switching or rapid mood switching and is a particularly treatment-resistant form of the disorder. ⮚ Fortunately, rapid cycling does not seem to be permanent, because only 3% to 5% of patients continue with rapid cycling across a 5-year period, with 80% returning to a non-rapid-cycling pattern within 2 years. Cyclothymic Disorder A milder but more chronic version of bipolar disorder called cyclothymic disorder is similar in many ways to persistent depressive disorder. Like persistent depressive disorder, cyclothymic disorder is a chronic alternation of mood elevation and depression that does not reach the severity of manic or major depressive episodes. Much of the time, such individuals are just considered moody. The average age of onset for bipolar I disorder is from 15 to 18 and for bipolar II disorder from 19 and 22, although cases of both can begin in childhood. Rates of completed suicide are 4 times higher in people with bipolar disorder than for people with recurrent major depression. The best estimates of the worldwide prevalence of mood disorders suggest that approximately 16% of the population experience major depressive disorder over a lifetime and approximately 6% have experienced a major depressive disorder in the last year. Studies indicate that women are twice as likely to have mood disorders as men, but the imbalance in prevalence between males and females is accounted for solely by major depressive disorder and persistent depressive disorder (dysthymia), because bipolar disorders are distributed approximately equally across gender. The general conclusion is that depressive disorders occur less often in prepubertal children than in adults but rise dramatically in adolescence. Major depressive disorder in adolescents is largely a female disorder, as it is in adults, with puberty seemingly triggering this sex imbalance. There is some evidence that 3-month-old babies can become depressed! Infants of depressed mothers display marked depressive behaviors (sad faces, slow movement, lack of responsiveness) even when interacting with a nondepressed adult. Childhood depression (and mania) is often associated with and sometimes misdiagnosed as attention deficit/hyperactivity disorder (ADHD) or, more often, conduct disorder in which aggression and even destructive behavior are common. But, once again, many of these children might now meet criteria for disruptive mood dysregulation disorder, which would better account for this comorbidity. Causes of Mood Disorders In family studies, we look at the prevalence of a given disorder in the first-degree relatives of an individual known to have the disorder (the proband). Increasing severity, recurrence of major depression, and earlier age of onset in the proband is associated with the highest rates of depression in relatives. A number of twin studies suggest that mood disorders are heritable. Note from the studies just described that bipolar disorder confers an increased risk of developing some mood disorder in close relatives, but not necessarily bipolar disorder. In other words, if one identical twin is unipolar, there is an 80% chance the other twin is unipolar as opposed to bipolar. In conclusion, the best estimates of genetic contributions to depression fall in the range of approximately 40% for women but seem to be significantly less for men (around 20%). Evidence supports the assumption of a close relationship among depression, anxiety, and panic (as well as other emotional disorders). Remember that the apparent primary function of serotonin is to regulate our emotional reactions. For example, we are more impulsive, and our moods swing more widely, when our levels of serotonin are low. Current thinking is that the balance of the various neurotransmitters and their interaction with systems of self-regulation are more important than the absolute level of any one neurotransmitter. In the context of this delicate balance, there is continued interest in the role of dopamine, particularly in relationship to manic episodes, atypical depression, or depression with psychotic features. For example, the dopamine agonist L-dopa seems to produce hypomania in bipolar patients, along with other dopamine agonists During the past several years, most attention has shifted away from a focus on neurotransmitters to the endocrine system and the “stress hypothesis” of the etiology of depression. This hypothesis focuses on overactivity in the hypothalamic–pituitary–adrenocortical (HPA) axis, which produces stress hormones. Investigators have also discovered that neurotransmitter activity in the hypothalamus regulates the release of hormones that affect the HPA axis. These neurohormones are an increasingly important focus of study in psychopathology. This connection led to the development of what was thought to be a biological test for depression, the dexamethasone suppression test (DST). ⮚ Dexamethasone is a glucocorticoid that suppresses cortisol secretion in normal participants. ⮚ When this substance was given to patients who were depressed, however, much less suppression was noticed than in normal participants, and what did occur didn’t last long. ⮚ However, later research demonstrated that individuals with other disorders, particularly anxiety disorders, also demonstrate nonsuppression, which eliminated its usefulness as a test to diagnose depression. Recognizing that stress hormones are elevated in patients with depression (and anxiety), researchers have begun to focus on the consequences of these elevations. Individuals experiencing heightened levels of stress hormones over a long period undergo some shrinkage of a brain structure called the hippocampus. But the new finding, at least in animals, is that long-term overproduction of stress hormones makes the organism unable to develop new neurons (neurogenesis). Thus, some theorists suspect that the connection between high stress hormones and depression is the suppression of neurogenesis in the hippocampus. Evidence reveals that healthy girls at risk for developing depression because their mothers suffer from recurrent depression have reduced hippocampal volume compared with girls with nondepressed mothers. This finding suggests that low hippocampal volume may precede and perhaps contribute to the onset of depression. Scientists have already observed that successful treatments for depression, including electroconvulsive therapy, seem to produce neurogenesis in the hippocampus, thereby reversing this process. More recently it has been demonstrated in animal laboratories that exercise increases neurogenesis, which could possibly be one mechanism of action in successful psychological treatments utilizing exercise, such as behavioral activation. Stress and trauma are among the most striking unique contributions to the etiology of all psychological disorders. Most people who develop depression report losing a job, getting divorced, having a child, or graduating from school and starting a career. But, as with most issues in the study of psychopathology, the significance of a major event is not easily discovered, so most investigators have stopped simply asking patients whether something bad (or good) happened and have begun to look at the context of the event, as well as the meaning it has for the individual. People become anxious and depressed when they decide that they have no control over the stress in their lives. These findings evolved into an important model called the learned helplessness theory of depression. ⮚ The depressive attributional style is (1) internal, in that the individual attributes negative events to personal failings (“it is all my fault”) ⮚ (2) stable, in that, even after a particular negative event passes, the attribution that “additional bad things will always be my fault” remains; and ⮚ (3) global, in that the attributions extend across a variety of issues. Aaron T. Beck suggested that depression may result from a tendency to interpret everyday events in a negative way. ⮚ Arbitrary inference is evident when a depressed individual emphasizes the negative rather than the positive aspects of a situation. A high school teacher may assume he is a terrible instructor because two students in his class fell asleep. He fails to consider other reasons they might be sleeping (up all night partying, perhaps) and “infers” that his teaching style is at fault. ⮚ As an example of overgeneralization, when your professor makes one critical remark on your paper, you then assume you will fail the class despite a long string of positive comments and good grades on other papers. ⮚ According to Beck, people who are depressed think like this all the time. They make cognitive errors in thinking negatively about themselves, their immediate world, and their future, three areas that together are called the depressive cognitive triad. ⮚ In a self-blame schema, individuals feel personally responsible for every bad thing that happens. ⮚ With a negative self-evaluation schema, they believe they can never do anything correctly. Although bipolar disorder is evenly divided between men and women, almost 70% of the individuals with major depressive disorder and dysthymia are women. Treatment of Mood Disorders Four basic types of antidepressant medications are used to treat depressive disorders: selective-serotonin reuptake inhibitors (SSRIs), mixed reuptake inhibitors, tricyclic antidepressants, and monoamine oxidase (MAO) inhibitors. Selective-serotonin reuptake inhibitors (SSRIs) specifically block the presynaptic reuptake of serotonin. This temporarily increases levels of serotonin at the receptor site, but again the precise longterm mechanism of action is unknown, although level