Psychological Disorders and Treatments ISC XII PDF
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C P Patel and F H Shah Commerce College
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This document explores psychological disorders and their treatments. It introduces the concept of a psychological disorder and defines it using the “four Ds”: deviance, distress, dysfunction, and danger. The document examines various perspectives on abnormal behavior, including biological, psychological, and socio-cultural factors. Finally, it presents the diathesis-stress model to explore how vulnerability and environmental stressors contribute to the development of mental illness.
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Page |1 PSYCHOLOGICAL DISORDERS AND TREATMENTS Abnormal Psychology The subfield of psychology that addresses the causes and progression of psychological disorders; also referred to as psychopathology. To determine whether someone has a psychological disorder we must first define...
Page |1 PSYCHOLOGICAL DISORDERS AND TREATMENTS Abnormal Psychology The subfield of psychology that addresses the causes and progression of psychological disorders; also referred to as psychopathology. To determine whether someone has a psychological disorder we must first define a psychological disorder: Psychological disorder A pattern of thoughts, feelings, or behaviours that causes significant personal distress, significant impairment in daily life, and/ or significant risk of harm, any of which is unusual for the context and culture in which it arises. Notice the word “significant” in the definition, which indicates that the diagnosis of psychological disorder is applied only when the symptoms have a substantial effect on a person’s life. As we shall see shortly all three elements (distress, impairment, and risk of harm) do not need to be present; if two (or even one) of the elements are present to a severe enough degree, then the person’s condition may merit the diagnosis of a psychological disorder. Although many definitions of abnormality have been used over the years, none has won universal acceptance. Still, most definitions have certain common features, often called the ‘four Ds’: deviance, distress, dysfunction, and danger. That is, psychological disorders are deviant (different, extreme, unusual, even bizarre), distressing (unpleasant and upsetting to the person and to others), dysfunctional (interfering with the person’s ability to carry out daily activities in a constructive way), and possibly dangerous (to the person or to others). This definition is a useful starting point from which we can explore psychological abnormality. Since the word ‘abnormal’ literally means “away from the normal,” it implies deviation from some clearly defined norms or standards. In psychology, we have no ‘ideal model’ or even ‘normal model’ of human behaviour to use as a base for comparison. Statistical stand It is no surprise that the state of mental health of a country, correlates positively with its economic growth. Projections show that India will suffer massive economic losses owing to mental health conditions. As of 2015, on a global level, over 322.48 million people worldwide suffer from some form of depressive disorder and as of 2017, more than 14 percent of the total population in India suffer from variations of mental disorders. The majority of this share includes older adult females in India. In India, every seventh person suffers from some form of mental disorder. The epidemiology of mental disorders, specifically, depression on a global scale, has been vastly studied. Today, it is regarded as the leading contributor to disease burden and morbidity worldwide, that may even result in suicide if left untreated. Risk factors, relative to Psychological disorders ISC XII Sakina Bhaigora Page |2 developing depressive and anxiety disorders, include bullying victimization, childhood sexual abuse, intimate partner violence, and lead exposure as an environmental risk factor which can lead to idiopathic developmental intellectual disability. One in seven Indians were affected by mental disorders of varying severity in 2017. The proportional contribution of mental disorders to the total disease burden in India has almost doubled since 1990. Substantial variations exist between states in the burden from different mental disorders and in their trends over time. These state-specific trends of each mental disorder reported here could guide appropriate policies and health system response to address the burden of mental disorders more effectively in India. Mental disorders are a diverse group of conditions varying in their presentation ranging from acute to recurrent to chronic, mild to severe, multiple disorders to single illness, morbid or co-morbid conditions and in several other ways. The prevalence of these disorders is also measured in number of ways like life time, past year, previous month and even in the last two weeks. Without the availability of objective tests for mental disorders, capturing precise estimates of these disorders in population-based surveys has always a been a challenge, globally; and will continue in the years to come. The prevalence rates of mental disorders are also critically influenced by a wide variety of factors, ranging from socio-economic and other environmental determinants, variations in perceived threshold of distress, differences in assessment tools, choice of symptom thresholds in disease definition and interpretations of results. Based on uniform and standardised data collection procedures from a nationally representative population, it is estimated that, excluding tobacco use disorders, mental morbidity of individuals above the age of 18 years currently was 10.6%. The lifetime prevalence in the surveyed population was 13.7%. This proportion of the population currently suffering from a mental disorder requires an active intervention. This estimate includes a range of mental disorders F10 – F49 categories within the International Classification of Disorders (ICD -10). Translated to real numbers (based on weightage for different levels), nearly 150 million Indians are in need of active interventions. The weighted prevalence across diagnostic categories in urban metros was higher than in rural and urban non-metro areas (with less than 10 million population). However, differences exist across diagnostic categories. The prevalence of schizophrenia and other psychoses (0.64%), mood disorders (5.6%) and neurotic or stress related disorders (6.93%) was nearly 2-3 times more in urban metros. One can speculate and consider the contribution of several factors (fast paced lifestyle, stress, complexities of living, breakdown of support systems, challenges of economic instability) for this higher prevalence and further investigations are needed to understand the relationship between urbanisation and mental illness. With continuing urbanisation, the burden is expected to rise and hence, there is a need for an urban specific mental health programme. While the causes, risk factors and protective factors vary in urban and rural populations, availability, accessibility, and affordability of mental health services as well as awareness are Psychological disorders ISC XII Sakina Bhaigora Page |3 major drivers of service utilisation. Thus, the need for coverage of mental health services across India on an equitable basis merits importance. Common mental disorders (CMDs), including depression, anxiety disorders and substance use disorders are a huge burden affecting nearly 10.0% of the population. This group of disorders are also intricately linked to both causation and consequences of several non- communicable disorders (NCD), thereby contributing to a significantly increased health burden. These disorders have previously been unaddressed in the planning and delivery of health care programmes. Individuals and families also ignore and neglect these disorders till they become severe. Different views of "abnormal" behaviour Approaches of how abnormal human behaviour is emphasized according to the biological, psychological, socio-cultural aspects: The viewing of mental disorder involves several perspectives that should be viewed as complementary to one another. Together these approaches provide a more accurate and complete picture of how such disorders arise and how they can be treated than any single perspective does alone. The biological model, emphasizes the role of the nervous system in mental disorders. This approach seeks to understand such disorders in terms of malfunctioning of portions of the brain, imbalances in various neurotransmitters and genetic factors. It is seen that many mental disorders show a high degree of concordance among close relatives. If one family member develops a disorder, then others are at increased risk for developing it too. The biological model has become increasingly influential in recent years as advances in neuroscience have revealed more and more about the role of various portions of the brain in many aspects of behaviour, and as techniques for observing the functioning of the brain (e.g. magnetic resonance imaging, PET scans) have improved. Psychological factors, too can be important. The psychological perspective emphasizes the role of basic psychological processes in the occurrence of mental disorders. For instance, many psychologists believe that learning plays a key role in many disorders. An example: phobias, or excessive fears of objects or situations. The psychological perspective also emphasizes the role of cognitive factors in mental disorders. For instance, many theories of depression suggest that long-lasting negative feelings often stem from faulty patterns of thoughts. The psychological perspective also takes account of unconscious forces and conflicts within individuals – the factors also vividly emphasized by Freud and his followers. Socio cultural factors do play a role in mental disorders. Psychologists and other mental health professionals believe that they do, and point to the important role of such social variables as poverty, unemployment, inferior education and prejudice as potential causes of at least some mental disorders. In other words, the socio-cultural perspective emphasizes the fact that external factors such as negative environments, a disadvantaged position in society, and cultural traditions can play a role in mental disorders In addition to these models, one of the most widely accepted explanations of abnormal behaviour has been provided by the diathesis-stress model. This model states that psychological disorders develop when a diathesis (biological predisposition to the disorder) is set off by a stressful situation. This model has three components. The first is the diathesis or the presence of some biological aberration which may be inherited. The second component is that the diathesis may carry a vulnerability to develop a psychological disorder. This means that the person is ‘at risk’ or ‘predisposed’ to develop the disorder. The third component is the presence of pathogenic stressors, i.e. factors/ stressors that may lead to psychopathology. If such “at risk” persons are exposed to these stressors, their predisposition may actually evolve into a disorder. This model has been applied to several disorders including anxiety, depression, and schizophrenia. This view suggests that mental disorders result from the joint effects of two influences: (1) a predisposition for a given disorder, termed a diathesis, and (2) stressors in an individual’s environment that tend to activate or stimulate the predisposition or vulnerability. In other words, the Psychological disorders ISC XII Sakina Bhaigora Page |4 diathesis–stress model suggests that for various reasons—genetic factors, early traumatic experiences, specific personality traits—individuals show varying degrees of vulnerability to specific mental disorders. Whether and to what extent an individual actually experiences such a disorder, however, depends on the environment in which the person lives. If the environment is favourable, the vulnerability (diathesis) may never be activated, and the person may never experience a mental disorder. If environmental factors are unfavourable, the diathesis may be activated, and one or more mental disorders may result. The Diagnostic Statistical Manual of Mental Disorders IV Diagnostic and Statistical Manual of Mental Disorders–IV (DSM–IV), published by the American Psychiatric Association (1994). Although this manual is published by the American Psychiatric Association, psychologists have long contributed to its development—and increasingly so in recent years. Thus, the manual is designed to help all mental health practitioners correctly identify (diagnose) specific disorders. The DSM-IV(TR) has also been published in 2000. The manual describes hundreds of specific disorders. These descriptions focus on observable features and include diagnostic features— symptoms that must be present before an individual is diagnosed as suffering from a particular problem. In addition, the manual also provides much additional background information on each disorder; for instance, information about biological factors associated with the condition and about variations in each disorder that may be related to age, cultural background, or gender. The American Psychiatric Association (APA) has published an official manual describing and classifying various kinds of psychological disorders. The current version of it, the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5), presents discrete clinical criteria which indicate the presence or absence of disorders. The classification scheme officially used in India and elsewhere is the tenth revision of the International Classification of Diseases (ICD-10), which is known as the ICD-10 Classification of Behavioural and Mental Disorders. It was prepared by the World Health Organisation (WHO). For each disorder, a description of the main clinical features or symptoms, and of other associated features including diagnostic guidelines is provided in this scheme. The DSM–IV classifies disorders along five axes rather than merely assigning them to a given category. This means that a person is described along several different dimensions (axes) rather than only one. Different axes relate to mental disorders, physical health, and social and occupational functioning. For our purposes, two of these axes are most important: Axis I, which relates to major disorders themselves, and Axis II, which relates to mental retardation and to personality disorders—extreme and inflexible personality traits that are distressing to the person or that cause problems in school, work, or interpersonal relationships. The third axis pertains to general medical conditions relevant to each disorder; the fourth axis considers psychosocial and environmental factors, including specific sources of Psychological disorders ISC XII Sakina Bhaigora Page |5 stress. Finally, the fifth axis relates to a global assessment of current functioning. By providing a system for evaluating people along each of these various axes, the DSM–IV helps clinicians gain a fuller picture of each patient’s current state and psychological functioning. By categorizing psychological disorders, clinicians and researchers can know more about a patient’s symptoms and about how to treat the patient. To be specific, classification systems of mental disorders provide the following benefits: They provide a type of shorthand, which enables clinicians and researchers to use a small number of words instead of lengthy descriptions. They allow clinicians and researchers to group certain abnormal thoughts, feelings, and behaviours into unique constellations. A particular diagnosis may also convey information about the etiology (causes) of the disorder, its course, and indications for its treatment. Classification systems also enable researchers to study the causes, the course, and the effects of treatments for various disorders. A diagnosis can indicate that an individual is in need of attention (including treatment), support, or benefits. Some people find great relief in learning that they are not alone in having particular problems. The first two axes specify the diagnosed disorders. Disorders listed on Axis I include most of the disorders in DSM-IV-TR and in this book, such as social phobia and bulimia nervosa. If an individual has comorbid Axis I disorders, all of the disorders are listed. For instance, if an individual has both social phobia and bulimia nervosa, both disorders would be listed on Axis I. Disorders listed on Axis II include mental retardation and personality disorders—personality traits that are so inflexible and self-defeating that they impair functioning. The authors of DSM-III’s multiaxial system believed that the presence of mental retardation or a personality disorder in a patient could significantly affect the expression of symptoms of other disorders— those on Axis I. Having a separate axis—Axis II— to specify such disorders ensures that these types of symptoms receive special attention. For example, suppose that a man who has moderate mental retardation lately seems to be “not himself”— he has been crying often, but when asked why, he says he does not know. His mental retardation makes it difficult for him to express himself well. The clinician diagnosing the man would need to determine how his mental retardation affects the way he expresses symptoms of a comorbid psychological disorder, such as depression or anxiety. Moreover, the presence of mental retardation may indicate that certain treatments would be more appropriate than others. On Axis III, mental health clinicians or researchers list any physical disorders or disabilities that might be relevant to the disorders on Axis I or II. For instance, an elderly woman with poor eyesight who recently suffered a hip fracture after a fall may now feel so anxious about leaving home that she has panic attacks— episodes of extreme fear, terror, or dread. To diagnose and treat this woman’s problems appropriately, a clinician would need to know about both her visual problems and her recent hip fracture; both medical problems would be noted on Axis III. The first three axes focus on current psychological and medical disorders. Axis IV focuses on the wider context of the disorder: social and environmental problems that could affect the diagnosis, treatment, and prognosis of a disorder. Knowing that a depressed patient’s mother recently died, for instance, may influence both the diagnosis and recommended treatment, if any. Social problems that affect a person’s psychological state are often called psychosocial problems. Such psychosocial and environmental problems include (American Psychiatric Association, 2000, pp. 31–32): 1. problems with the person’s primary support group (e.g., marital conflict or divorce, or some type of maltreatment); 2. problems with the social environment (e.g., the death of a friend or discrimination); 3. educational problems (e.g., academic problems or difficulties with a teacher); 4. occupational problems (e.g., unemployment or stressful working conditions); 5. housing problems (e.g., homelessness or an unsafe neighbourhood); 6. economic problems (e.g., extreme poverty); 7. problems with access to health care (e.g., inadequate health insurance or lack of transportation to health care facilities); and Psychological disorders ISC XII Sakina Bhaigora Page |6 8. legal difficulties (e.g., being arrested or being a victim of a crime). Axis V requires the clinician or researcher to provide a numerical estimate (between 1 and 100) of the patient’s global functioning within the past year, a high number indicates a proficient level of functioning the patient has achieved in his or her work, relationships, and leisure time or the patient’s current level of functioning. This information can be used to plan treatment and estimate the level of functioning likely to be attained after treatment. Is the DSM–IV a useful tool for psychologists? In several ways, it is. It appears to be higher in reliability than earlier versions, and it rests more firmly on careful empirical research. However, it’s important to note that it is still largely descriptive in nature: It describes psychological disorders, but it makes no attempt to explain them. This is deliberate; the DSM–IV was specifically designed to assist in diagnosis. It remains neutral with respect to various theories about the origins of psychological disorders. Because psychology as a science seeks explanation, not simply description, however, many psychologists view this aspect of the DSM–IV as a shortcoming that limits its value. In addition, the DSM–IV attaches specific labels to people, and this may activate stereotypes about them. Once a person is labelled as showing a particular mental disorder, psychologists and mental health professionals may perceive the person largely in terms of that label; and this may lead them to overlook important information about the person. A third criticism is that the DSM–IV may be gender-biased. Females are diagnosed as showing certain disorders much more frequently than males, and some critics suggest that this is due to the fact that the DSM–IV descriptions of these disorders seem to reflect society’s views about women (sex-role stereotypes). Finally, the DSM–IV has been criticized because mental disorders occur on a continuum, not in discrete categories. People don’t necessarily simply have or not have a disorder; they may have the disorder to various degrees, and may show different aspects of it in varying proportions. For this reason, many psychologists prefer a dimensional approach, in which individuals are not simply assigned to specific categories but rather are rated on many different dimensions, each relevant to a specific mental disorder. Still, although many psychologists might prefer a dimensional approach, and although they recognize the other potential problems with the DSM–IV already noted, they continue to use the manual because of the benefits of having a single widely used framework for describing and discussing mental disorders. Anxiety Disorders Anxiety: Increased arousal accompanied by generalized feelings of fear or apprehension. Anxiety Disorders: Psychological disorders that take several different forms, but which are all related to a generalized feeling of anxiety. Psychological disorders ISC XII Sakina Bhaigora Page |7 Everyone has worries and fears. The term anxiety is usually defined as a diffuse, vague, very unpleasant feeling of fear and apprehension. The anxious individual also shows combinations of the following symptoms: rapid heart rate, shortness of breath, diarrhoea, loss of appetite, fainting, dizziness, sweating, sleeplessness, frequent urination and tremors. There are many types of anxiety disorders. They include generalised anxiety disorder, which consists of prolonged, vague, unexplained and intense fears that are not attached to any particular object. The symptoms include worry and apprehensive feelings about the future; hypervigilance, which involves constantly scanning the environment for dangers. It is marked by motor tension, as a result of which the person is unable to relax, is restless, and visibly shaky and tense. We experience anxiety when we are waiting to take an examination, or to visit a dentist, or even to give a solo performance. This is normal and expected and even motivates us to do our task well. On the other hand, high levels of anxiety that are distressing and interfere with effective functioning indicate the presence of an anxiety disorder — the most common category of psychological disorders. Everyone has worries and fears. The term anxiety is usually defined as a diffuse, vague, very unpleasant feeling of fear and apprehension. The anxious individual also shows combinations of the following symptoms: rapid heart rate, shortness of breath, diarrhoea, loss of appetite, fainting, dizziness, sweating, sleeplessness, frequent urination, and tremors. Generalized anxiety disorder (GAD) Generalized anxiety disorder (GAD) is characterized by uncontrollable worry and anxiety about a number of events or activities (which are not solely the focus of another Axis I disorder, such as about having a panic attack). The worry and anxiety among individuals suffering from GAD primarily focus on family, finances, work, and illness (Sanderson & Barlow, 1990); Earl Campbell worried mostly about family and illness; other people may worry about minor matters (Craske, Rapee, Jackel, & Barlow, 1989). In contrast to most people, people with GAD worry even when things are going well. Moreover, their worries intrude into their awareness when they are trying to focus on other thoughts—and they cannot stop worrying (American Psychiatric Association, 2000). Symptoms are present for at least half the days during a 6-month period. Generalized anxiety disorder (GAD) The anxiety disorder characterized by uncontrollable worry and anxiety about a number of events or activities that are not solely the focus of another Axis I disorder. Because the symptoms are chronic (lasting at least 6 months) and because many people with GAD can usually function adequately in some areas of their daily lives, they come to see their worrying and anxiety as a part of themselves, not as a disorder. The worrying may be so intrusive that people feel restless, have difficulty concentrating or sleeping, and become irritable. Causes The brain ultimately controls the body’s responses, and thus GAD must involve the brain in some way. However, researchers are only beginning to identify the precise ways in which large-scale brain mechanisms are altered to produce GAD (Nutt, 2001). For example, they have found that patients with GAD have more gray and white matter in the superior temporal gyrus, an area used in hearing and language comprehension, than do individuals who do not have this disorder. The role of the right hemisphere was also evident in an fMRI study in which adolescent patients with GAD and adolescents in a control group viewed angry and neutral faces (Monk et al., 2006). The researchers found that a key part of the right Psychological disorders ISC XII Sakina Bhaigora Page |8 frontal lobe was more strongly activated for the patients than for the controls when the participants saw angry faces. However, patients who showed greater activation in this area had less severe anxiety. GAD is associated with decreased arousal that arises from an unusually responsive parasympathetic nervous system. The parasympathetic nervous system tends to cause effects opposite to those caused by the sympathetic nervous system. So, for instance, heightened parasympathetic activity slows heart rate, stimulates digestion and the bladder, and causes pupils to contract (Barlow, 2002a). When an individual with GAD perceives a threatening stimulus, his or her subsequent worry temporarily reduces any arousal (Borkovec & Hu, 1990), suppresses negative emotions. Although the frontal lobes of patients with GAD are normal in size, the dopamine in the frontal lobes of these patients does not function normally (Stein, Westenberg, & Liebowitz, 2002). In fact, numerous studies suggest that a wide range of neurotransmitters, including gamma-aminobutyric acid (GABA), serotonin, and norepinephrine, may not function properly in people with GAD (Nutt, 2001). These neurotransmitters affect, among other things, people’s response to reward, their motivation, and how effectively they can pay attention to stimuli and events. Studies of the genetics of GAD have produced solid evidence that GAD has a genetic component. The heritability estimate for GAD is at least 15–20% (Hettema, Prescott, & Kendler, 2001) and possibly almost 40% (Scherrer et al., 2000) and the disorder is equally heritable for men and women (Hettema, Prescott, & Kendler, 2001). Stressful life events, such as a death in the family, friction in a close relationship, or trouble on the job, can trigger symptoms of GAD in someone who is neurologically and psychologically vulnerable to developing it. For people who develop GAD after age 40, the disorder often arises after a significant stressor occurs. GAD also appears to be related more directly to relationships. In one interesting study, researchers found that college students with GAD rated themselves as having more severe global relationship problems (often being too compliant and deferential to others) than did college students in a control group. However, when friends of the students with GAD and friends of the control participants were asked to rate the severity of relationship problems of the participants in the study, the ratings did not differ for the GAD and control participants (Eng & Heimberg, 2006). This means that the GAD students felt that they had problems with relationships, but people close to them did not see it that way. People with GAD may experience increased stress if they view themselves as having serious problems in relationships. Increased stress, in turn, can lead to distress and negative emotions that can be difficult to manage and regulate (Mennin, Turk et al., 2004). Phobias You might have met or heard of someone who was afraid to travel in a lift or climb to the tenth floor of a building or refused to enter a room if s/he saw a lizard. You may have also felt it yourself or seen a friend unable to speak a word of a well-memorised and rehearsed speech before an audience. These kinds of fears are termed as phobias. People who have phobias have irrational fears related to specific objects, people, or Psychological disorders ISC XII Sakina Bhaigora Page |9 situations. Phobias often develop gradually or begin with a generalised anxiety disorder. Phobias can be grouped into three main types, i.e. specific phobias, social phobias, and agoraphobia. Specific phobias are the most commonly occurring type of phobia. This group includes irrational fears such as intense fear of a certain type of animal, or of being in an enclosed space. Intense and incapacitating fear and embarrassment when dealing with others characterises social anxiety disorder (social phobia). Social phobia (Social Anxiety Disorder) Social phobia, also called social anxiety disorder, is an intense fear of public humiliation or embarrassment, together with the avoidance of social situations likely to cause this fear (American Psychiatric Association, 2000). Such social situations often include those where a person could be judged—for instance, public speaking. Social phobia may also arise in social situations in which most people would not think twice about being judged, such as eating in the presence of others or using public restrooms or dressing rooms. People with social phobia avoid such situations whenever possible—and may even avoid making eye contact with other people. When a social situation cannot be avoided and must be endured, the person with social phobia experiences panic or anxiety, sometimes including symptoms of upset stomach, diarrhoea, sweating, muscle tension, and heart palpitations. DSM-IV-TR distinguishes between a social phobia that is limited to specific social performances where the individual is the center of attention—such as making a presentation—and generalized social phobia, which leads a person to fear and avoid all social situations. People who have social phobia also tend to be extremely sensitive to criticism and rejection and to worry about not living up to the perceived expectations of others. Thus, they often dread being evaluated or taking tests, and they may not perform up to their potential at school or work. Unfortunately, their diminished performance challenges their self-esteem, increasing their anxiety during subsequent performances or tests. Similarly, achievement at work may suffer because they avoid social situations that are important for advancement on the job, such as making presentations. People with social phobia are less likely to marry or have a partner than people who do not have this disorder. People with severe social phobia may quit school and be unable to get a job because the social interactions required at school or work are more than they feel they can endure. Sometimes, a clinician or researcher cannot easily distinguish whether an individual’s symptoms indicate that he or she has a social phobia or panic disorder with agoraphobia. However, there are two key features that distinguish these disorders: 1. People with social phobia fear other people’s scrutiny. 2. People with social phobia rarely have panic attacks when alone. Causes Social phobia involves fear, and researchers have shown repeatedly that the amygdala is strongly activated when animals—including humans—are afraid (Rosen & Donley, 2006). Thus, it is no surprise that the amygdala is more strongly activated when people with social phobia see faces with negative expressions (such as anger) than when they see happy faces, and that this difference is greater than observed in control participants who do not have the disorder (Phan et al., 2006). In addition, the more symptoms of social phobia a person has, the more strongly the amygdala is activated when the person views faces with negative expressions. Researchers have shown that a number of brain areas, including the hippocampus Psychological disorders ISC XII Sakina Bhaigora P a g e | 10 and cortical areas near it, do not function normally in people who have the disorder (Furmark et al., 2002). Moreover, the right hemisphere appears to play a part in this disorder, which is not surprising, given its role in withdrawal emotions. Virtually all of the major neurotransmitters may function abnormally in individuals who have social phobia, but impaired dopamine activity may be particularly important (Li, Chokka, & Tibbo, 2001). Researchers have examined regions of the brain that rely on dopamine and found that patients with social phobia show less activation in these regions than do control participants. But dopamine dysfunction cannot be the whole story; for example, evidence that people with social phobia have too little serotonin may suggest why SSRIs have sometimes been found to help these patients (Gorman & Kent, 1999; Lykouras, 1999). As is the norm for anxiety disorders, social phobia appears to arise from both genetic factors and environmental factors (Mathew, Caplan, & Groman, 2001; Stein, Jang, & Livesley, 2002). The heritability of social phobia is about 37% on average (with a range of 12–60% in numerous studies) (Beatty et al., 2002; Fyer, 2000; Kendler et al., 1992; Li, Chokka, & Tibbo, 2001; Neale et al., 1994). Furthermore, we noted earlier that some people with social phobia were extremely shy as children; they had what is called a shy temperament, or behavioural inhibition (Biederman et al., 2001; Kagan, 1989), which has a genetic component. These patients cannot really be said to have developed a phobia, since they always had a basic level of discomfort in particular social situations (Coupland, 2001). People who have social phobia have particular biases in attention and memory (Ledley & Heimberg, 2006; Lundh & Öst, 1996; Wenzel & Cochran, 2006). At the outset of one study, participants were shown photos of faces and asked to judge each facial expression as critical or accepting (Lundh & Öst, 1996). Following this, they were shown a larger set of faces and asked to pick out the ones that they had been shown initially. Those with social phobia were more likely to recognize the faces that they had earlier judged as critical, whereas those without social phobia were more likely to recognize faces that they had judged as accepting. Thus, people with social phobia seem to pay more attention to—and hence better remember—faces that they perceive as critical, which in turn feeds into their fears about being evaluated. Similarly, cognitive distortions about the world can lead people with social phobia to see it as an extremely dangerous place; they then become chronically hypervigilant for potential social threats and negative evaluations by others (Beck & Emery, 1985; Joorman & Gotlib, 2006; Rapee & Heimberg, 1997). In some cases, classical conditioning can contribute to the development of social phobia: A social situation (the conditioned stimulus) becomes paired with a negative social experience (such as public humiliation) to produce a conditioned emotional response (Mineka & Zinbarg, 1995). The conditioned response (fear or anxiety) may generalize to other, or even all, types of social situations. Operant conditioning principles apply to social phobia as well: a person with social phobia might avoid social situations in order to decrease the probability of an uncomfortable experience. The avoidant behaviour does decrease anxiety and is thus reinforced (Mowrer, 1939). Social factors that contribute to social phobia include the message some children receive from their interactions with family members—that social interactions can be a threat—and the influence of culture Psychological disorders ISC XII Sakina Bhaigora P a g e | 11 on people’s concerns and fears about social interactions. Extreme overprotection by parents is associated with childhood anxiety (Hudson & Rapee, 2001; Wiborg & Dahl, 1997); such overprotection may lead children to cope with their anxiety through avoidance (Barrett et al., 1996). In certain Asian cultures, such as those of Korea and Japan, a person with social phobia may be especially afraid of offending others; in particular, he or she may fear that his or her body odor or blushing will be offensive. In Japan, this fear is known as taijin kyofusho (Dinnel, Kleinknecht, & Tanaka- Matsumi, 2002; Guarnaccia, 1997a). This contrasts with a fear among North Americans and Europeans of being humiliated by something they say or do (Lee & Oh, 1999). Specific phobias DSM-IV-TR describes the central element of a specific phobia as an excessive or unreasonable anxiety or fear related to a specific situation or object (American Psychiatric Association, 2000). People with a specific phobia know that their fear is excessive or unreasonable. A person with a specific phobia works hard to avoid the feared stimulus, often significantly restricting his or her activity in the process. A person with an elevator phobia, for example, will choose to walk up many flights of stairs rather than take the elevator. Specific phobias you might recognize include claustrophobia (fear of small spaces), arachnophobia (spiders), and acrophobia (heights). DSM-IV-TR lists five types or categories of specific phobias: animal, natural environment, blood-injection-injury, situational, and “other” (American Psychiatric Association, 2000).The animal type of specific phobia pertains to an extreme fear or avoidance of any variety of animal; commonly feared animals include snakes and spiders. Symptoms of the animal type of specific phobia usually emerge in childhood. People with a phobia for one kind of animal often also have a phobia for another kind of animal. a. The natural environment type of specific phobia typically focuses on heights, water, or storms. b. The blood-injection-injury type of specific phobia produces a strong response to seeing blood, having injections, sustaining bodily injuries, or watching surgery. This type of phobia runs in families and emerges in early childhood. A unique response of this specific phobia involves first an increased arousal, then a rapid decrease in heart. rate and blood pressure, which often causes fainting. Among people with this type of phobia, over half report having fainted in response to a feared stimulus (Öst, 1992). c. A situational type of specific phobia involves a fear of a particular situation, such as being in an airplane, elevator, or enclosed space, or of driving a car. Some people develop this type of phobia in childhood, but in general it has a later onset, often in the mid-20s. People with this type tend to experience more panic attacks than do people with other types of specific phobia (Lipsitz et al., 2002). d. This category includes any other type of specific phobia that does not fall into the four categories already discussed. Examples of specific phobias that would be classified as “other” are a fear of falling down when not near a wall or some other type of support, a fear of costumed characters (such as clowns at a circus), and a phobic avoidance of situations that may lead to choking, vomiting, or contracting an illness. Psychological disorders ISC XII Sakina Bhaigora P a g e | 12 Causes The amygdala appears to have a hair-trigger in patients with specific phobia. For example, in one fMRI study, patients who were phobic of spiders and control participants were asked to match geometric figures. In one PET study, people who had phobias of animals were shown pictures of those animals (e.g., snakes) while their brains were scanned (Rauch et al., 1995). The photos of animals not only activated various parts of the limbic system (including the amygdala), but also activated the part of the cortex (known as somatosensory cortex) that registers sensations on the body. The sort of anxiety evoked by specific phobias is associated with too little of the inhibitory neurotransmitter substance GABA (File, Gonzalez, & Gallant, 1999). In addition, lower levels of the neurotransmitter acetylcholine are associated with higher levels of anxiety (Degroot & Treit, 2002). Moreover, the systems that produce acetylcholine and serotonin appear to be linked, so that increases in the output of one are accompanied by decreases in the output of the other (File, Kenny, & Cheeta, 2000); thus, reducing the serotonin level raises the level of acetylcholine, which in turn decreases anxiety. Moreover, to make the situation even more complicated, norepinephrine is also implicated in anxiety. Researchers have discovered that some genes predispose individuals to develop a specific phobia (but not a particular one), whereas other genes underlie each specific type of phobia (Kendler et al., 2001; Lichtenstein & Annas, 2000). People who have a specific phobia have a particular cognitive bias—they believe strongly that something bad will happen when they encounter the feared stimulus (Tomarken, Mineka, & Cook, 1989). They also overestimate the probability that an unpleasant event, such as falling from a high place or an airplane’s crashing into a tall building, will occur (Pauli, Wiedemann, & Montoya, 1998). People who have a specific phobia may also have perceptual distortions related to their feared stimulus. For example, a person with a spider phobia may perceive that a spider is moving straight toward him or her when it is not (Riskind, Moore, & Bowley, 1995). From a learning perspective, classical conditioning and operant conditioning could account for the development and maintenance of a specific phobia. Watson and Rayner’s conditioning of Little Albert’s fear of rats was the first experimental induction of a classically conditioned phobia. Avoidance of the feared stimulus is negatively reinforced (Mowrer, 1939): The feared stimulus causes anxiety, which is then relieved by avoiding the stimulus. Sometimes, simply seeing other people exhibit fear of a particular stimulus is enough to make the observer become afraid of that stimulus (Mineka, Cook, & Miller, 1984). For example, if as a young child, you saw your older cousin become agitated and anxious when a dog approached, you might well learn to do the same. Similarly, repeated warnings about the dangers of a stimulus can increase the risk of developing a specific phobia of that stimulus (Antony & Barlow, 2002). After hearing about a plane crash on the news, it is no surprise that some people became afraid to fly— even though they had not been in a plane accident themselves. Modeling is not the only way that culture can exert an effect on the content of specific phobias. Consider the fact that people in India are twice as likely as people in England to have phobias of animals, darkness, and harsh weather. Psychological disorders ISC XII Sakina Bhaigora P a g e | 13 Separation anxiety disorder (SAD) Separation anxiety disorder (SAD) is another type of anxiety disorder. Individuals with separation anxiety disorder are fearful and anxious about separation from attachment figures to an extent that is developmentally not appropriate. Children with SAD may have difficulty being in a room by themselves, going to school alone, are fearful of entering new situations, and cling to and shadow their parents’ every move. To avoid separation, children with SAD may fuss, scream, throw severe tantrums, or make suicidal gestures. Separation Anxiety Disorder: extreme distress when expecting or going through separation from home or other significant people to whom the individual is immensely attached to. Separation anxiety is more than a child’s getting upset about temporarily saying goodbye to a parent. Children with separation anxiety disorder may become so homesick when away from home that activities—such as a sleepover at a friend’s or a stay at overnight camp—are interrupted in order to return home. Or these children may want to always know the parent’s whereabouts, using a cell phone to make frequent contact during any physical separation. And when away from the parent, they may also manifest physical symptoms of anxiety dizziness, stomach-aches, nausea and vomiting, and feeling faint. Separation anxiety disorder most commonly arises in children who are part of tightknit families (American Psychiatric Association, 2000). Separation anxiety disorder is more common among first- degree relatives (parents and siblings) than in the general population, and the disorder is considered to be moderately heritable (Cronk et al., 2004). However, the heritability probably reflects a heritability of anxiety in general: Separation anxiety is more common among children whose mothers have panic disorder than among children whose mothers don’t have that disorder (Cronk et al., 2004). But other factors create feedback loops: Tight-knit families may reinforce behaviours associated with anxiety about separation and may punish behaviours associated with actual separation. If so, then children in such families who have temperaments that are high in harm avoidance and reward dependence may be especially vulnerable, because they will be relatively responsive to reward and punishment. Moreover, separation anxiety disorder is more common in children whose fathers are absent (Cronk et al., 2004), perhaps because that absence leads the child to have a heightened fear of losing the remaining parent. Obsessive Compulsive Disorder People affected by obsessive-compulsive disorder are unable to control their preoccupation with specific ideas or are unable to prevent themselves from repeatedly carrying out a particular act or series of acts that affect their ability to carry out normal activities. Obsessive behaviour is the inability to stop thinking about a particular idea or topic. The person involved, often finds these thoughts to be unpleasant and shameful. Compulsive behaviour is the need to perform certain behaviours over and over again. Many compulsions deal with counting, ordering, checking, touching and washing. Other disorders in this category include hoarding disorder, trichotillomania (hair-pulling disorder), excoriation (skin-picking) disorder etc. People affected by obsessive-compulsive disorder are unable to control their preoccupation with specific ideas or are unable to prevent themselves from repeatedly carrying out a particular act or series of acts that affect their ability to carry out normal activities. Obsessive behaviour is the inability to stop Psychological disorders ISC XII Sakina Bhaigora P a g e | 14 thinking about a particular idea or topic. The person involved, often finds these thoughts to be unpleasant and shameful. Compulsive behaviour is the need to perform certain behaviours over and over again. Many compulsions deal with counting, ordering, checking, touching, and washing. Other disorders in this category include hoarding disorder, trichotillomania (hair-pulling disorder), excoriation (skin-picking) disorder etc. Obsessions are thoughts, impulses, or images that persist or recur, are intrusive—and therefore difficult to ignore—and are inappropriate to the situation (American Psychiatric Association, 2000). Whereas obsessions involve thoughts, impulses, and images, compulsions involve behaviours. A compulsion is a repetitive behaviour (such as avoiding stepping on sidewalk cracks) or mental act (such as silently counting to 10) that a person feels driven to carry out; a compulsion usually corresponds thematically to an obsession. The key element of obsessive-compulsive disorder (OCD) is one or more obsessions, which may occur together with compulsions (American Psychiatric Association, 2000). The obsession can cause great distress and anxiety, despite a person’s attempts to ignore or drive out the intrusive thoughts. People with OCD recognize that their obsessive thoughts do not originate from an external source—for example, the thoughts are not implanted by aliens from outer space, as some people with psychotic symptoms believe. Instead, they realize that the thoughts arise in their own minds, even though they cannot control or suppress the thoughts. Obsessions include preoccupations with contamination, order, fear of losing control, doubts about whether the patient performed an action, and possible needs. Compulsive behaviours are usually related to an obsession or anxiety associated with a particular situation or stimulus and include washing, ordering, counting, checking, and hoarding (Mataix- Cols, do Rosario-Campos, & Leckman, 2005). Performing the behaviour temporarily prevents or relieves the anxiety. However, compulsions that relieve a Psychological disorders ISC XII Sakina Bhaigora P a g e | 15 nxiety can take significant amounts of time to complete—sometimes more than an hour—and often create distress or impair functioning. DSM-IV-TR does not include subtypes of OCD. Like the other anxiety disorders, we have discussed, OCD often involves an unrealistic or disproportionate fear—in this case, of adverse consequences if the compulsive behaviour is not completed. For instance, someone who hoards newspapers may be afraid that if she did not keep the papers, she would be unable to find an article that might later be crucial in some unforeseen medical or legal matter. Causes When the frontal lobes trigger an action, there is feedback from the basal ganglia—and sometimes this feedback sets up a loop of repetitive activity. Many researchers now believe that this neural loop plays a key role in obsessive thoughts, which intrude and cannot be stopped easily. Performing a compulsion might temporarily stop the obsessive thoughts by reducing the repetitive neural activity (Insel, 1992; Jenike, 1984; Modell et al., 1989). (But soon after the compulsive behaviour stops, the obsessions typically resume.) Consistent with these ideas, Rapoport (1991) proposed that OCD symptoms can be caused by dysfunctional connections among the frontal lobes, the thalamus, and the basal ganglia. Much research has focused on possible abnormalities in the basal ganglia and frontal lobesin particular (Insel, 1992; Pigott, Myers, & Williams, 1996; Saxena & Rauch, 2000). In fact, as predicted by the theory, both the frontal cortex (especially the orbital frontal cortex—the lower parts of the cortex, behind the eyes) and the basal ganglia function abnormally in OCD patients (Baxter, 1992; Berthier et al., 2001; Saxena et al., 1998). This abnormal functioning could well prevent the frontal lobe from cutting off the loop of repetitive neural activity, as it appears to do in normal people. Researchers have also suggested that OCD is associated with larger amounts of gray matter in the frontal lobes and smaller amounts in the posterior portions of the brain (Kim et al., 2001). Such structural abnormalities are consistent with the unusually large amount of activity in patients’ frontal regions when they see a stimulus that provokes the OCD-related thoughts and behaviours (Adler et al., 2000). Furthermore, these patients have impaired visual-spatial abilities, which rely on similar areas of the brain (Micallef & Blin, 2001). In fact, researchers have found that many (but not all) patients with OCD had an abnormal birth, epilepsy, head trauma, or infection of the brain or the membranes that cover it. One reason may be that people with OCD have too little of the neurotransmitter serotonin, which allows unusual brain activity to occur (Mundo et al., 2000). Twin studies have shown that if one monozygotic (identical) twin has OCD, the other is likely (65%) to have it. As should be expected if this high rate reflects common genes, the rate is lower (only 15%) for dizygotic twins (Pauls, Raymond, & Robertson, 1991). Moreover, as you would expect from the results of the twin studies, OCD is more common among relatives of OCD patients (10.3% of whom also have OCD) than among relatives of control participants (of whom only 2% also have OCD) (Pauls et al., 1995). Compulsive behaviour can provide short-term relief from anxiety that is produced by an obsession. Operant conditioning occurs when the behaviour is negatively reinforced: Because it (temporarily) relieves the anxiety, it is more likely to recur when the thoughts arise again. One theory about how a normal obsession becomes part of OCD is that the person decides that his or her thoughts refer to something unacceptable, such as killing someone or, catching someone else’s illness (Salkovskis, 1985). These obsessive thoughts, which the individual believes imply some kind of danger, lead to extremely Psychological disorders ISC XII Sakina Bhaigora P a g e | 16 uncomfortable feelings. Mental or behavioural rituals arise in order to reduce these feelings. A related theory is that for some people who develop OCD, a disturbing thought is the moral equivalent of actually performing the act, which leads to greater distress in response to the initial obsession (Rachman, 1997; Shafran, Thordarson, & Rachman, 1996). Both theories contrast a normal response to “unacceptable” thoughts (an awareness that such thoughts do not need to be controlled and an ability to let them fade from consciousness) with the belief of OCD patients that such thoughts must be controlled—and trying to do so amplifies the thoughts (Tolin, Worhunsky, & Maltby, 2006). The onset of OCD often follows a stressor, and the severity of the symptoms is often proportional to the severity of the stressor (Turner & Beidel, 1988), which might range from taking a vacation at one end to the death of a family member at the other. However, such fi ndings are not always easy to interpret. For example, one study found that people with more severe OCD tend to have more kinds of family stress and are more likely to be rejected by their families (Calvocoressi et al., 1995). Although stress in the family may cause the greater severity of symptoms, it is also possible that the more severe symptoms led the families to reject the patients. In fact, a more recent study found that the more severe the patient’s OCD symptoms, the less hopeful and more depressed were family members (Geffken et al., 2006). People with OCD often impose various restrictions on the behaviour of friends and family members to ensure that it conforms to the patient’s “rules.” Different countries have about the same prevalence rates of OCD, although culture (Weissman et al., 1994) and religion can help determine the particular content of some obsessions or compulsions. For instance, religious obsessions and praying compulsions are more common among Turkish men than French men (Millet et al., 2000) and more common among Brazilians than Americans or Europeans (Fontenelle et al., 2004). And a devoutly religious patient’s symptoms can relate to the specific tenets and practices of his or her religion (Shooka et al., 1998): Someone who is Catholic may have obsessional worries about having impure thoughts or feel a compulsion to go to confession multiple times each day. In contrast, devout Jews or Muslims may have symptoms that focus on extreme adherence to religious dietary laws. Depression One of the most widely prevalent and recognised of all mental disorders is depression. Depression covers a variety of negative moods and behavioural changes. Depression can refer to a symptom or a disorder. In day-to- day life, we often use the term depression to refer to normal feelings after a significant loss, such as the break-up of a relationship, or the failure to attain a significant goal. Major depressive disorder is defined as a period of depressed mood and/or loss of interest or pleasure in most activities, together with other symptoms which may include change in body weight, constant sleep problems, tiredness, inability to think clearly, agitation, greatly slowed behaviour, and thoughts of death and suicide. Other symptoms include excessive guilt or feelings of worthlessness. Psychological disorders ISC XII Sakina Bhaigora P a g e | 17 Factors Predisposing towards Depression: Genetic make-up, or heredity is an important risk factor for major depression and other depressive disorders. Age is also a risk factor. For instance, women are particularly at risk during young adulthood, while for men the risk is highest in early middle age. Similarly gender also plays a significant role in this differential risk addition. For example, women in comparison to men are more likely to report a depressive disorder. Other risk factors are experiencing negative life events and lack of social support. A clinician who uses the DSM-IV-TR system to categorize mood disorders builds a diagnosis based on a person’s current and past history of episodes of disturbed moods. For depressive disorders, there is only one building block: major depressive episode (MDE), which is characterized by severe depression that lasts for at least 2 weeks. MDE is not itself a diagnosis, but a building block toward a diagnosis (as we shall see later in this chapter, the diagnosis for other disorders typically requires several building blocks). Mood (which is a type of affect) is not the only symptom of a major depressive episode. Behaviour and cognition are also affected by depression. These three spheres of functioning are sometimes referred to as the ABCs— affect, behaviour, and cognition (but should not be confused with the ABCs of behaviour therapy— antecedent, behaviour, consequence). During a major depressive episode, a person can feel unremitting sadness, hopelessness, or numbness. Some people also suffer from a loss of pleasure, referred to as anhedonia, a state in which activities and intellectual pursuits that were once enjoyable no longer are, or at least are not nearly as enjoyable as they had been. Someone who liked to go to the movies, for instance, may no longer find it so interesting or fun and may feel that it is not worth the effort. Anhedonia can thus lead to social withdrawal. Other mood related symptoms of depression include weepiness—crying at the drop of a hat or for no apparent reason—and decreased sexual interest or desire. People who are depressed make more negative comments, make less eye contact, are less responsive, speak more softly, and speak in shorter sentences than people who are not depressed (Gotlib & Robinson, 1982; Segrin & Abramson, 1994). Depression is also evident behaviourally in one of two ways: psychomotor agitation or psychomotor retardation. Psychomotor agitation is an inability to sit still, evidenced by pacing, hand wringing, or rubbing or pulling the skin, clothes, or other objects. In contrast, psychomotor retardation is a slowing of motor functions indicated by slowed bodily movements and speech (in particular, longer pauses in answering) and lower volume, variety, or amount of speech. These two psychomotor symptoms, along with changes in appetite, weight, and sleep, are classified as vegetative signs of depression. Sleep changes can involve insomnia or, less commonly, hypersomnia, which is sleeping more hours each day than normal. In addition, people who are depressed may feel less energetic than usual or feel tired or fatigued even when they do not physically exert themselves. In fact, many people who are depressed had sleep disturbances up to a month before the depression began, which suggests that sleep irregularities may be a harbinger of a depressive episode (Perlis et al., 1997; Perlis, Smith, et al., 2006). When in the grip of depression, people often feel worthless or guilt-ridden, may evaluate themselves negatively for no objective reason, and tend to ruminate over their past failings (which they may exaggerate). They may misinterpret ambiguous statements made by other people as evidence of their worthlessness. Depressed patients can also feel unwarranted responsibility for negative events, to the point of having delusions that revolve around an intense sense of guilt, deserved punishment, worthlessness, or personal responsibility for problems in the world. They blame themselves for their depression and for the fact that they cannot function well. During a depressive episode, people may also report difficulty thinking, remembering, concentrating, and making decisions. According to DSM-IV-TR, once someone’s symptoms meet the criteria for a major depressive episode, he or she is diagnosed as having major depressive disorder (MDD)—five or more symptoms of an MDE lasting more than 2 weeks. Unfortunately, more than half of those who have had a single depressive episode go on to have at least one additional episode, noted in DSM-IV-TR as MDD, recurrent depression. Some people have increasingly frequent episodes over time, others have clusters of episodes, and still others have isolated depressive episodes followed by several years without symptoms (American Psychiatric Association, 2000; McGrath et al., 2006). Research suggests that periods of remission last longer earlier in life. That is, as people with recurrent MDD grow older, they are free of depression for increasingly shorter periods (American Psychiatric Association, 2000). Causes Studies of depressed people have shown that they have unusually low activity in a part of the frontal lobe that has direct connections to the amygdala (which is involved in fear and other strong emotions) and to Psychological disorders ISC XII Sakina Bhaigora P a g e | 18 other brain areas involved in emotion (Kennedy et al., 1997). The depressed brain is not as able as the normal brain to regulate emotion. Moreover, this part of the frontal lobe has connections to the brain areas that produce the neurotransmitter substances dopamine, serotonin, and norepinephrine. Thus, this part of the frontal lobe may well be involved in regulating the amounts of such substances. This is important because these substances are involved in reward and emotion, which again hints that the brains of these people are not regulating emotion normally. Researchers have refined this general observation and reported that one aspect of depression—lack of motivated behaviour—is specifically related to reduced activity in the frontal (and parietal) lobes (Milak et al., 2005). In addition, these researchers report that depression does not simply reflect that the brain as a whole has become sluggish. Rather, they found that more severe depression is associated with greater activity in the emotion-related limbic system, which fits with the idea that emotions are not being effectively regulated. Moreover, these researchers found that some of the brain areas involved in attention (in particular, the thalamus) and in controlling movements (basal ganglia) are overactive in depressed people, which again suggests that the functions carried out by these brain areas are not being regulated normally. Researchers have long known that the symptoms of depression can be alleviated by medications that alter the activity of serotonin or norepinephrine (Arana & Rosenbaum, 2000). One of the early attempts to explain depression in terms of a single neurotransmitter is called the catecholamine hypothesis, which posits that symptoms of depression arise when levels of norepinephrine fall too low (Schildkraut, 1965). Support for this hypothesis came from studies showing that people who are depressed have fewer by- products of norepinephrine in their urine and cerebrospinal fluid (Nemeroff, 1998). Perhaps surprisingly, however, autopsies of the brains of people who were depressed found that many of them had a higher than normal density of norepinephrine receptors (Meana, Barturen, & Garcia-Sevilla, 1992). This apparent paradox is resolved by knowing that when the brain does not produce enough of a neurotransmitter, it often attempts to compensate by increasing the number of receptors that respond to it. An increase in the number of receptors allows a given amount of neurotransmitter to have a larger effect. Dopamine also appears to play several roles in depression (Nutt, 2008); too little of it not only can undermine the effects of reward (and hence can lead to lack of pleasure), but also can produce psychomotor retardation (Clausius, Born & Grunz, 2009; Martin-Soelch, 2009; Stein, 2008). In short, depression involves not only norepinephrine, but also serotonin and dopamine—and perhaps other neurotransmitters as well. Nemeroff (1998, 2008) formulated the stress–diathesis model of depression. The stress– diathesis model of depression focuses specifically on the hypothalamic-pituitary-adrenal axis and the role of cortisol, a hormone that is secreted in larger amounts when an individual experiences stress. According to the stress– diathesis model, people with depression have an excess of cortisol circulating in their blood, which makes their brains prone to overreacting when they experience stress. Twin studies show that when one twin of a monozygotic (identical) pair has MDD, the other twin has a risk of also developing the disorder that is four times higher than when the twins are dizygotic (fraternal; Bowman & Nurnberger, 1993; Kendler, Karkowski, & Prescott, 1999). Because monozygotic twins basically share all of their genes but dizygotic Psychological disorders ISC XII Sakina Bhaigora P a g e | 19 twins share only half of their genes, these results point to a role for genetics in the etiology of this disorder. One possibility is that genes influence how a person responds to stressful events (Costello et al., 2002; Kendler et al., 2005). People who are depressed are more likely to pay attention to sad and angry faces than to faces that display positive emotions (Gotlib, Kasch, et al., 2004; Gotlib, Krasnoperova, et al., 2004; Leyman et al., 2007); people who do not have a psychological disorder spend equal time looking at faces those express different emotions. This attentional bias has also been found for negative words and scenes, as well as for remembering depression-related—versus neutral—stimuli (Caseras et al., 2007; Gotlib, Kasch, et al., 2004; Matt, Vasquez, & Campbell, 1992; Mogg, Bradley, & Williams, 1995). Such an attentional bias may leave depressed people more sensitive to other people’s sad moods and to negative feedback from others (or even a lack of positive feedback, as occurs when a person fails to smile when greeting you), compounding their depressive thoughts and feelings. Aaron Beck proposed that cognitive distortions are the root cause of many disorders. Beck (1967) has suggested that people with depression tend to have overly negative views about (1) the world, (2) the self, and (3) the future, referred to as the negative triad of depression. These distorted views can cause and maintain chronically depressed feelings and depression-related behaviours. For instance, a man who does not get the big raise he hoped for might respond with cognitive distortions that give rise to dysfunctional thoughts. He might think that he is not “successful” because he did not get the raise, and therefore that he must be worthless (notice the circular reasoning). This man is more likely to become depressed than he would be if he did not have such dysfunctional thoughts. While experiencing negative emotions, some people reflect on these emotions; during such ruminations, they might say to themselves: “Why do terrible things always happen to me?” or “Why did they say those hurtful things about me—is it something I did?” or “Should I have spoken more during the discussion?” (Nolen- Hoeksema & Morrow, 1991). Such ruminative thinking has been linked to depression (Just & Alloy, 1997; Nolen-Hoeksema, 2000; Nolen-Hoeksema & Morrow, 1991, 1993). Studies have examined the relationship between depression and specific forms of rumination, such as stress-reactive rumination, which is ruminating about negative implications of stressful life events. Researchers assess this type of rumination by asking participants to agree or disagree with statements about what they “generally do when feeling down, sad, or depressed.” Examples of such statements include: “Think about how the stressful event was all your fault” “Think about what the occurrence of the stressor means about you” “Think about how things like this always happen to you” (Robinson & Alloy, 2003). In general, people who consistently attribute negative events to their own qualities—called an internal attributional style—are more likely to become depressed. In one study, mothers-to-be who had an internal attributional style were more likely to be depressed 3 months after childbirth than were mothers-to-be who had an external attributional style—blaming negative events on qualities of others or on the environment (Peterson & Seligman, 1984). Similarly, college students who tended to blame themselves, rather than external factors for negative events, were more likely than those who did not to become depressed after receiving a bad grade (Metalsky et al., 1993). Three particular aspects of attributions are related to depression: whether the attributions are internal or external, stable (enduring causes) or unstable (local, transient causes), and global (general, overall causes) or specific (particular, precise causes). Individuals who tend to attribute ne