Untitled Flashcards Set

Chapter 11 - Eating Disorders

Chapter Outline:

- Clinical Description of Eating Disorders

- Etiology of Eating Disorders

- Treatment of Eating Disorders

Anorexia Nervosa

• In the DSM-5

◦ Restriction of food that leads to very low body weight; body weight is significantly

below normal

◦ Intense fear of weight gain or repeated behaviors to interfere with weight gain

◦ Body image disturbance

• Weight loss is typically achieved through dieting

◦ Can also occur through purging and excessive exercise

• Fear of gaining weight is not reduced by weight loss

• Even when emancipated, those with anorexia nervosa may believe they are overweight

◦ They overestimate their body size

◦ They will choose a thin figure as ideal

• Severity ratings are based on Body Mass Index (BMI)

SUBTYPES OF ANOREXIA NERVOSA

• Restricting type

◦ Weight loss is achieved by severely limiting food intake

• Binge-eating/purging type

◦ The person has also regularly engaged in binge eating and purging

• Longitudinal research suggests limited validity, yet clinical utility of subtypes

EPIDEMIOLOGY

• Onset: early to middle teenage years

• Usually triggered by dieting and stress

• At least 3x more frequent in women than men

• Often comorbid with depression, OCD, phobias, panic, and/or personality disorders

• Suicide rates are high

◦ 5% completing

◦ 20% attempting

PHYSICAL CONSEQUENCES

• Low blood pressure, heart rate decreases

• Kidney and gastrointestinal problems

• Loss of bone mass

• Brittle nails, dry skin, hair loss

• Lanugo (a fine, soft hair) may develop

• Altered levels of potassium and sodium electrolytes

◦ Can cause tiredness, weakness, and sudden death

PROGNOSIS

• 50-70% eventually recover

◦ May often take 6 or 7 years

◦ Relapse is common

• Difficult to modify distorted view of self, especially in cultures that highly value thinness

• Anorexia is life-threatening

◦ Death rates are 10x higher than general population

◦ Death rates are 2x higher than other psychological disorders

◦ Death often results from physical complications of the illness

Bulimia Nervosa

• In the DSM-5:

◦ Recurrent episodes of binge-eating

◦ Recurrent compensatory behaviors to prevent weight gain

✦ e.g., purging (vomiting), fasting, excessive exercise, use of laxatives and/or diuretics

◦ Body shape and weight are extremely important in self-evaluation

Table 11.4 Severity Ratings for Bulimia Nervosa in

DSM-5

RATING NO. OF COMPENSATORY BEHAVIORS

Mild 1-3 compensatory behaviors/week

Moderate 4-7

Severe 8-13

Extreme 14 or more

• A binge episode includes:

◦ An excessive amount of food consumed in a short period of time; A feeling of losing

control over eating

• Typically occurs in secret

• May be triggered by stress, negative emotions or negative social interractions

◦ Typical food choices: Cakes, cookies, ice cream, other easily consumed high-calorie

foods

◦ Avoiding a craved food can later increase likelihood of binge; Reports of losing

awareness/dissociation

◦ Shame and remorse often follow

• Compensatory behaviors include:

◦ Feelings of discomfort, disgust, and fear of weight gain lead to an inappropriate

compensatory behavior

✦ Attempt to undo the caloric effects of the binge

◦ Vomiting, laxative, and diuretic abuse, fasting, excessive exercise are used to prevent

weight gain

◦ Binge/purge episode must occur at least once a week for 3 months

EPIDEMIOLOGY

• Onset: late adolescence or early adulthood

• 90% of people with bulimia nervosa are women

• Prevalence among women is 1-2%

• Typically overweight before onset and symptoms begin while dieting

• Comorbid with depression, personality disorders, anxiety, substance use disorders,

conduct disorder

• Suicide rates are higher than in general population

◦ But much lower than in anorexia nervosa

PHYSICAL CONSEQUENCES

• Potassium depletion from purging

• Laxative use depletes electrolytes, which can cause cardiac irregularities

• Vomiting may lead to tearing of the tissues in the stomach and throat

• Loss of dental enamel from stomach acids in vomit

• Mortality rate is higher than in other disorders

PROGNOSIS

• Approx. 75% recover

• 10-20% remain fully symptomatic

• Early intervention linked with improved outcomes

• Poorer prognosis when depression and substance abuse are comorbid or when more

severe symptomatology

Bulimia vs. Anorexia

The key difference is weight loss. People with anorexia nervosa lose a tremendous

amount of weight, people with bulimia nervosa do not.

Binge Eating Disorders

• In the DSM-5: (includes at least 3 of the ff)

◦ Eating more quickly than usual; Eating until over full

◦ Eating large amounts even if not hungry

◦ Eating alone due to embarrassment about large food quantity

◦ Feeling bad (e.g., disgusted, guilty, or depressed) after the binge

• Recurrent binge eating episodes

• No compensatory behavior is present

Table 11.5 Severity for Binge Eating Disorder in DSM-5

RATING NO. OF BINGES

Mild 1-3 binges/week

Moderate 4-7

Severe 8-13

Extreme 14 or more

EPIDEMIOLOGY

• Associated with obesity and history of dieting

◦ BMI > 30

• Comorbid with mood disorders, anxiety disorders, ADHD, conduct disorder, and

substance use disorders

• Risk factors include:

◦ Childhood obesity, critical comments about being overweight, weight-loss attempts in

childhood, low self-concept, depression, and childhood physical or sexual abuse

• More prevalent in women

• More prevalent than anorexia or bulimia

• Equally prevalent among Euro-, African-, Asian-, and Hispanic-Americans

PHYSICAL CONSEQUENCES

• Problems associated with obesity:

◦ Increased risk of type 2 diabetes

◦ Cardiovascular problems

◦ Chronic back pain

◦ Headaches

• Problems independent of obesity:

◦ Sleep problems

◦ Anxiety/depression

◦ Irritable bowel syndrome

◦ Early onset of menstruation in women

PROGNOSIS

• This is a relatively new diagnosis

◦ New to DSM-5

◦ Few studies have assessed prognosis

• Research so far suggests between 25-82% recover

• Duration of just over 4 years

Binge Eating Disorder vs. Anorexia and Bulimia

vs. Anorexia Nervosa

-

absence of weight loss in binge eating disorders

vs. Bulimia Nervosa

-

exercise) in binge eating disorder

absence of compensatory behaviors (purging, fasting, or excessive

Two Subtypes of Eating Disorders:

Pica Disorder

- The desire to consume non-edible ‘foods’

- Usually present in children

Rumination Disorder

- Consuming food, vomitting it, then eating it again

- Characterized by regurgitation of food and consumption directly after and it is not

something that the person wants to do, it’s involuntary

Etiology of Eating Disorders

GENETIC INFLUENCES

• First-degree relatives of women with:

◦ Anorexia, are 10x more likely to have the disorder

◦ Bulimia, are 4x more likely to have the disorder

• First-degree relatives appear to be at higher risk

• Higher MZ (monozygote) concordance rates for both anorexia and bulimia

• Nonshared environmental factors also contribute to the development of eating disorders

• Key features: body dissatisfaction, desire for thinness, binge eating and weight

preoccupation, are heritable

NEUROBIOLOGICAL INFLUENCES

• Hypothalamus

◦ Regulates hunger and eating

◦ However, it does not seem a likely causal factor in anorexia nervosa

• Low levels of endogenous opioids

◦ Substances that reduce pain, enhance mood, and suppress appetite

◦ Released during starvation

✦ May reinforce restricted eating of anorexia

◦ Excessive exercise also increases opioids

• Serotonin

◦ Related to feelings of satiety (fullness)

◦ Low levels of serotonin metabolites among people with anorexia and bulimia suggests

underactive serotonin activity

◦ Antidepressants that increase serotonin often effective in treatment of eating disorders

✦ May be linked to comorbid depression

• Dopamine

◦ Incentive-Sensitization Theory

✦ Related to feelings of pleasure and motivation

✦ Dopamine plays a key role in “liking” of food and the “wanting” or craving of food

COGNITIVE BEHAVIORAL FACTORS

• Anorexia Nervosa

◦ Body-image disturbance powerfully reinforces weight loss

◦ Behaviors that achieve or maintain thinness:

✦ Negatively reinforced by the reduction of anxiety about gaining weight

✦ Positively reinforced by comments from others; by the sense of mastery or self-control

◦ Low Positive Emotion Differentiation

✦ Involves a diminished ability to distinguish between discrete positive emotions

◦ Perfectionism and personal inadequacy lead to excessive concern about weight

◦ Criticism from family and peers

• Bulimia Nervosa

◦ Self-worth strongly influenced by weight and shape

◦ Lapses in rigid restrictive eating rules escalates into a binge

◦ After binging, disgust with oneself and fear of gaining weight lead to compensatory

behavior

◦ Purging temporarily reduces anxiety about weight gain

◦ This cycle lowers a person’s self-esteem, which triggers further bingeing and purging

◦ Schematic of Cognitive Behavior Theory of Bulimia Nervosa

✦ Low self-esteem and high negative affect —> dieting to feel better about self —> food

intake is restricted too severely —> diet is broken —> binge —> compensatory

behaviors to reduce fears of weight gain

• Binge Eating

◦ People with bulimia nervosa and binge eating disorder

✦ Typically binge when under stress or experience negative emotions

✦ Propensity to experience negative emotions predicts the onset of eating disorders

✦ Binging may function as a way to regulate emotion

✦ However, people with these disorders often feel more negative after a binge

SOCIOCULTURAL FACTORS

• The cultural ideal has progressed steadily toward increasing thinness

• Dieting, especially among women, has become more prevalent; often precedes onset

• Higher BMI and body dissatisfaction is related to higher risk for developing eating

disorders

• Unrealistic media portrayals

◦ Women may feel shame when they don’t match the ideal; “Pro-eating disorder”

websites

• Stigma associated with being overweight

• Gender Influences

◦ Objectification of women’s bodies

✦ Women defined by their bodies; men defined by their accomplishments

✦ Societal objectification of women leads to “self-objectification”

✧ Women see their own bodies through the eyes of others

✧ Leads to more shame when they fall short of cultural ideals

◦ Aging and changes in life roles

✦ Having a life partner or having children associated with decreases in eating disorder

symptoms

• Cross-Cultural Factors

◦ Anorexia found in many cultures

✦ Even those with little Western cultural influence

✦ May not include fears of getting fat

◦ As countries become more like Western cultures, eating disorders increase

◦ Bulimia more common in industrialized societies than non-industrialized ones

OTHER INFLUENCES

• Personality Influences

◦ Severe restriction of food intake can have powerful effects on personality and behaviour

✦ Preoccupation with food, fatigue, poor concentration, lack of sexual interest,

irritability, moodiness, and insomnia

◦ Personality characteristics before an eating disorder

✦ Body dissatisfaction, poor interoceptive awareness, and negative affect predicted

disordered eating

✦ Perfectionism high among women with anorexia and remains high after successful

treatment

• Family characteristics

◦ Self-reports of people with eating disorders indicate high levels of family conflict

✦ Parental reports don’t always indicate family problems

◦ One observational study:

✦ No difference in frequency of positive and negative message among parents with and

without a child with an eating disorder

◦ More observational studies needed

Treatments of Eating Disorders

MEDICATIONS

• Anorexia Nervosa

◦ Medications have been used with little success in improving weight or other core

features of anorexia

• Bulimia Nervosa

◦ Often treated with antidepressants

✦ Likely because it is often comorbid with depression

◦ Dropouts and relapse rates high

• Binge Eating Disorder

◦ Limited research suggests that antidepressant medications are not effective in reducing

binges or increasing weight loss

PSYCHOLOGICAL TREATMENT

• Anorexia Nervosa

◦ Immediate goal is to increase weight to avoid medical complications and avoid death

◦ Second goal is long-term maintenance of weight gain

◦ CBT: Reductions in symptoms through 1 year

◦ Family-based therapy (FBT)

✦ Interactions among family members

✦ Helps parents support child’s healthy weight

✦ Early results show improved outcomes over individual therapy; Early weight gain may

be an important predictor of a good outcomes

• Bulimia Nervosa

◦ CBT is the primary treatment

✦ Best-validated and most current standard for treatment

✦ Challenges societal standards for physical attractiveness

✦ Challenges beliefs about weight and dieting

✦ Challenge all-or-nothing beliefs about food

✦ Increase self-assertiveness skills

✦ Increase regular eating patterns (three meals per day)

◦ CBT is more effective than medication

✦ Adding medication may help alleviate depression

✦ Adding exposure and ritual prevention (ERP) may not add much beyond CBT alone

◦ Guided self-help CBT

✦ Use of self-help books on topics such as perfectionism, body image, negative

thinking, and food and health

✦ Meet for small number of sessions with a therapist to guide them through self-help

material

◦ Interpersonal therapy: Not as effective in the short-term as CBT

• Bing Eating Disorder

◦ CBT is shown to be effective

✦ Targets binge eating through self-monitoring, self-control, and problem-solving skills

◦ CBT is more effective than medication

◦ Interpersonal therapy equally as effective as CBT and guided self-help CBT

✦ All three are more effective than behavioral weight-loss programs

✦ Behavioral weight-loss programs promote weight loss, but do not curb binge eating

PREVENTION OF EATING DISORDERS

• Psychoeducational approaches

◦ Early education about eating disorders

• Deemphasize sociocultural influences

◦ Help resist or reject sociocultural pressures to be thin

• Risk-factor approach

◦ Identify people at risk (e.g., weight and body-image concern, restricting food) and

intervene to alter these factors

Chapter 8 - Dissociative

Disorders and Somatic

Symptom-Related Disorders

Chapter Outline

- Clinical Descriptions and Epidemiology of the Dissociative Disorders (DID)

- Etiology of DID

- Treatment of DID

- Clinical Description of Somatic Symptom and Related Disorders

- Etiology of Somatic Symptom and Related Disorders

Depersonalization/

derealization disorder

Experience of detachment from the self and reality

Dissociative amnesia Lack of conscious access to memory, typically of a stressful

experience. The fugue sybtype involves traveling or wandering

coupled with the loss of memory of one’s identity or past.

Dissociative identity

disorder

At least two distinct personalities that act independently of each

other

Overview Dissociative Disorders:

• Dissociation

◦ Some aspect of emotion, memory, or experience being inaccessible consciously

◦ Some types of dissociation are common (e.g., losing track of time)

• What causes dissociation?

◦ Psychodynamic and behavioral theorists

✦ An avoidance response that protects the person from consciously experiencing

stressful events

◦ Trauma and sleep disturbance

Depersonalization/Derealization Disorder

• Disconcerting and disruptive sense of detachment from one’s self and surroundings

• Depersonalization

◦ A sense of detachment from one’s self or surroundings

◦ e.g., being an observer outside one’s body

• Derealization

◦ A sense of detachment from one’s surroundings

• Symptoms are:

◦ Persistent or recurrent

◦ Does not involve disturbance of memory

◦ Symptoms usually triggered by stress

◦ Usually begins in adolescence

◦ Comorbid personality disorders are frequent

✦ 90% will experience anxiety

◦ Childhood trauma is often reported

◦ Can co-occur with other disorders

✦ Symptoms should not be entirely explained by other disorders

• In the DSM-5:

◦ Depersonalization: Experiences of detachment from one’s mental processes or body, as

though one is in a dream, or

◦ Derealization: Experiences of unreality of surroundings

◦ Symptoms are persistent or recurrent

◦ Reality testing remains intact

◦ Symptoms are not explained by substances, another dissociative disorder, another

psychological disoder, or by a medical condition

Etiology of Depersonalization/Derealization Disorder:

• Linked to problems in integrating sensory and bodily information — brain integration

issues

◦ Atypical brain activity in sensory intergration areas (visual, auditory, somatosensory) in

patients with depersonalization/derealization disorder

• Anterior cingulate cortex is underactive in patients with disorder when viewing emotionally

evocative images, potentially causing affective numbness

• Things that can trigger it:

◦ Mismatched sensory experiences can induce the disorder in individuals without it

✦ e.g., distorted visual information

• Mismatched neural signals from bodily sensory cues

Dissociative Amnesia

• Inability to recall important personal information, usually about a traumatic experience

◦ Typically occurs after severe stress

◦ Too extensive to be ordinary forgetfulness

◦ May last several hours to several years

◦ Usually disappears as suddenly as it began, with complete recovery of memory

◦ Other behavior is unremarkable

◦ Procedural memory remains intact

• Rule out other common causes of memory loss:

◦ Substance abuse, brain injury, medication side effects

◦ Dementia - memory fails slowly over time; is not linked to stress

◦ Accompanied by inability to learn new information

• What causes dissociative amnesia?

◦ Psychodynamic Theory: Traumatic events are repressed

◦ Cognitive Theory: Stress enhances encoding of central features of negative events; High

levels of stress hormones and chronic stress interfere with memory formation

DISSOCIATIVE FUGUE SUBTYPE

• Most severe subtype, extensive memory loss

• Person typically disappears from home and work

◦ May assume a new identity

✦ new name, job, personality characteristics

• Recovery is usually complete

• People are able to remember details of their life

◦ Except for those events that took place durring the fugue

• In the DSM-5:

◦ Inability to remember important autobiographical information, usually of a traumatic or

stressful nature, that is too extensive to be ordinary forgetfulness

◦ The amnesia is not explained by substances, or by other medical or psychological

conditions

◦ Specify dissociative fugue subtype if amnesia is associated with bewildered or

apparently purposeful wandering

Dissociative Identity Disorder (DID)

• A person has at least 2 separate personalities (alters)

◦ Each has different modes of being, thinking, feeling, and acting

◦ Alters exist independently or one another

◦ Alters emerge at different times

◦ Primary alter may be unaware of existence of other alters; may have no memory of what

other alters do

• Usually the primary alter seeks treatment

• Most commonly. 2-4 alters are identified when diagnosed

• Rarely diagnosed until adulthood

◦ Symptoms may date back to childhood

• Moore common in women than men

• Other diagnoses are often present

◦ PTSD, Major Depressive Disorder, Somatic Symptom Disorders, Personality Disorders

• Other common symptoms:

◦ Headaches, hallucinations, suicide attempts, self-injurious behaviors, amnesia,

depersonalization

• In the DSM-5:

◦ Disruption of identity characterrized by two or more distinct personality states (alters) or

an experience of possession

◦ These disruptions lead to discontinuities in the sense of self or agency, as reflected in

altered cognition, behavior, affect, perceptions, consciousness, memories, or sensory-

motor functioning

◦ This disruption may be observed by others or reported by the patient

◦ Recurrent gaps in memory for events or important personal information that are beyond

orrdinary forgetting

◦ Symptoms are not part of a broadly accepted cultural or religious practice

◦ Symptoms are not due to drugs or a medical condition

◦ In children, symptoms are not better explained by an imaginary playmate or by fantasy

play

Etiology of Dissociative Identity Disorder:

POSSTRAUMATIC MODEL

• Some people are particularly likely to use dissociation to cope with trauma

• Children who are abused are at risk for developing dissociative symptoms

• Children who dissociate are more likely to develop psychological symptoms after trauma

SOCIOCOGNITIVE MODEL

• People who have been abused seek explanations for their symptoms and distress

• Alters appear in response to suggestions by:

◦ Therapists; Exposure to media reports of DID; Other cultural influences

• DID could be iatrogenic (created within treatment)

◦ Reinforcement of identified alters and suggestive techniques might promote symptoms

in vulnerable people

◦ Not viewed as conscious deception

• Evidence in support of the Sociocognitive Model:

◦ The symptoms of DID can be role-played

◦ Some therapists reinforce DID symptoms

✦ Use of hypnosis, urging clients to unbury unremembered abuse experiences, naming

different alters

✦ Most clients are unaware of having alters before treatment progresses

◦ Alters share memories, even when they report amnesia

✦ Implicit memories are transferred between alters

The Epidemiology of Dissociative Disorders

• Reports of lifetime diagnostic criteria for:

◦ Depersonalization/derealization: 2.5%

◦ Dissociative amnesia: 7.5%

◦ Dissociative ideentity disorder: 1-3%

◦ Likely overestimations due to measurement issues

• No identified reports of DID or dissociative amnesia before the 1800s

• Increased rates since the 1970s

◦ Appearance of DID in popular culture

✦ DSM-III (1980) defined DID for the first time

Treatments

• No well-validated treatments available

• No randomized controlled trials have assesed psychological treatment

• Medications have not been shown to relieve DID symptoms

PSYCHODYNAMIC TREATMENT

• DID is believed to arise from traumatic events that the person is trying to block from

consciousness

• Goal: Overcome repression

• Use of hypnosis

◦ Age regression - person is encouraged to go back in his or her mind to traumatic events

in childhood

◦ Can actually worsen symptoms

Somatic Symptom and Related Disorders (SSRD)

• Excessive concerns about physical symptoms or health: Tendency to seek frequent

medical treatment

◦ Often see several physicians for a given health concern

◦ May try different drugs; Hospitalization and surgery are common experiences

• Criticisms of diagnostic criteria: Conditions are so varied; Patients often find these

diagnoses stigmatizing

• Tend to co-occur with anxiety disorders, mood disorders, and personality disorders

• Distress over symptoms is authentic

Somatic symptom

disorder

Excessive thought, distress, and behavior related to somatic

symptoms

Illness anxiety disorder Unwarranted fears about a serious illness in the absence of any

significant somatic symptoms

Conversion disorder Neurological symptom(s) that cannot be explained by medical

disease or culturally sanctioned behavior

Malingering Intentionally faking psychological or somatic symptoms to gain

from these symptoms

Factitious disorder Falsification of psychological or physical symptoms, without

evidence of gains from those symptoms

• In the DSM-5:

◦ At least one somatic symptom that is distressing or disrupts daily life

◦ Duration of at least 6 months

◦ Specify if predominant pain

◦ Excessive thoughts, distress, and behaviors related to somatic symptom(s) or health

concerns, as indicated by at least one of the following:

✦ Health-related anxiety; Disproportionate and persistent concerns about the

seriousness of symptoms; Excessive time and energy devoted to health concerns

Somatic Symptom Disorder

• Distress revolves around a somatic symptom that exists

• Can be diagnosed regardless of whether symptoms can be explained medically

• When psychological factors are the cause of symptoms, an alternative DSM diagnosis,

Psychological Factors Affecting Other Medical Conditions, may be appropriately

considered

Illness Anxiety Disorder

• Preoccupation with and high level of anxiety about having or acquiring a serious disease

• Excessive behaviors (e.g., checking for signs of illness, seeking reassurance) or

maladaptive avoidance (e.g., avoiding medical car)

• No more than mild somatic symptoms are present

• Not explained by other psychological disorders

• Preoccupation lasts at least 6 months

• Preoccupation with fears of having a serious disease despite having no significant

somatic symptoms

• Easily alarmed about their health

• May be haunted by visual images of becoming ill or dying

• May react with anxiety when they hear about illnesses in their friends or the community

• Fears are not easily calmed

◦ May become frustrated when attempts to sooth worries fail

Conversion Disorder

• One or more symptoms affecting voluntary motor or sensory function

• The symptoms are incompatible with recognized medical disorders

• Symptoms cause significant distress or functional impairment or warrant medical

evaluation

• Sudden development of neurological symptoms:

◦ Partial or complete paralysis of arms or legs

◦ Seizures or coordination problems

◦ Vision impairment or tunnel vision

◦ Anesthesia: Insensitivity to pain

◦ Aphonia: Whispered speech

• The symptoms suggest an illness related to neurological damage

• Medical tests indicate that the bodily organs and nervous system are fine

• Genuinely physical problems are misdiagnosed as conversion disorder about 4% of the

time

• Many people with conversion disorder show no signs that they are amplifying their

symptoms

• Onset typically adolescence or early adulthood

◦ Onset is usually rapid

• Prevalence less than 1%

◦ More common in women than men

◦ Highly likely to meet criteria for another somatic symptom disorder

Malingering Disorder

• A person intentionally fakes a symptom to avoid responsibility or to achieve some reward

• The symptoms are under voluntary control

Factitious Disorder

• People intentionally produce symptoms to assume the role of a patient

• Symptoms are mostly physical but some produce psychological symptoms as well

◦ People make themselves ill by intentional injury, taking damaging medications, etc.

• May be diagnosed in a parent who creates a physical illness in a child

◦ ex. deedee and gypsy rose blanchard

Etiology of Somatic Symptom-Related Disorders

• These disorders do not appear to be heritable

• Little is known about the etiology of the DSM-5 somatic symptom-related disorders

◦ Most researchers use DSM-IV-TR diagnoses

✦ DSM-5 and DSM-IV-TR differ considerably

◦ Focus on neurobiological and cognitive behavioral models

✦ Excessive attention to somatic symptoms

✦ Disproportionate anxiety about one’s health

NEUROBIOLOGICAL FACTORS

• Anterior insula and anterior cingulate cortex

◦ Brain regions activated by unpleasant body sensations

• Somatosensory cortex

◦ Brain region involved with processing bodily sensations

• Heightened activity in these regions is related to greater propensity for somatic symptoms

• Pain and somatic symptoms can be increased by anxiety, depression, and stress

hormones

COGNITIVE BEHAVIORAL FACTORS

• Two important cognitive variables:

◦ Attention to bodily sensations

✦ Automatic focus on physical health cues

◦ Interpretation of those sensations

✦ Overreact with overly negative interpretations

• Behavioral consequences of fear of impending illness:

◦ Assuming the sick role, which intensifies poor health

◦ Safety behaviors (e.g., help-seeking)

✦ Prevents extinction of fear

✦ Maintains focus on potential health concerns

Etiology of Conversion Disorder:

PSYCHODYNAMIC AND NEUROSCIENCE PERSPECTIVES

• Psychodynamic

◦ Physical symptom is a response to an unconscious psychological conflict

• Neuroscience

◦ Much of our perceptual processing may operate outside of our conscious awareness

SOCIAL AND CULTURAL FACTORS

• More common among people:

◦ From rural areas

◦ Of lower SES

• Social factors (e.g., modeling), shape how conversion symptoms unfold

Treatment of Conversion Disorder

MAJOR OBSTACLES

• Most people with somatic symptom-related disorders want medical care

◦ Not mental health care

• Referral to mental health may be viewed as invalidating

• A reminder of the mind-body connection can enhance their willingness to consider

psychological treatment

TRAIN MEDICAL PROFESSIONALS

• Teach primary care teams to tailor care for people with somatic symptom-related

disorders

• Alert physicians when a patient is an intensive user of health care services

COGNITIVE BEHAVIORAL STRATEGIES

• Identify and change triggering emotions

• Change cognitions about symptoms

• Change behaviors to improve social interactions

• Train people to pay less attention to their body

• Help people resume healthy activities and rebuild life

• Involve family members to reduce attention given to somatic symptoms

• Mindfulness Treatments

• Two small randomized controlled trials indicate beneficial effects of CBT for specific forms

of conversion disorder:

◦ Explanation that medical tests had not revealed an explanation for symptoms

◦ Patients were reinforced for taking part in physical training to improve area of difficulty

◦ Treatment team ignored ongoing signs of conversion symptoms.

Chapter 9 - Schizophrenia

Chapter Outline:

- Clinical Descriptions of Schizophrenia

- Etiology of Schizophrenia

- Treatment of Schizophrenia

Schizophrenia

- originally called “demential praecox” but changed to schizo (“schizein” meaning “to

split”) and phrenia (“phren” meaning “mind)

• Influences the way a person thinks, feels, behaves

◦ Disordered thinking

✦ Ideas not logically related

◦ Faulty perception and attention

◦ Lack of emotional expressiveness

◦ Disturbances in movement or behavior

• Widespread disruptions in life: Maintaining jobs, living independently, having close

relationships

• Substance use, suicide, and mortality rates are high

Epidemiology

• Lifetime prevalence is 1%

• Affects men slightly more often than women

• Onset typically in late adolescence/early adulthood

◦ Men diagnosed at a slightly earlier age

• Often experience several acute episodes with less severe symtpoms between episodes

Symptoms

There are 3 major clusters of symptoms: Positive, Negative, Disorganized

Positive Symptoms Negative Symptoms Disorganized Symptoms

Delusions, hallucinations Avolition, alogia, anhedonia,

blunted affect, asociality

Disorganized behavior,

disorganized speech

• POSITIVE SYMPTOMS (DELUSIONS)

◦ Beliefs contrary to reality

◦ Firmly held despite disconfirming evidence

◦ Types of delusions:

✦ Thought insertion

✦ Thought broadcasting

✦ Feelings or behaviors are controlled by external force

✦ Grandiose delusions

✦ Ideas of reference

• POSITIVE SYMPTOMS (HALLUCINATIONS)

◦ Sensory experiences in the absence of sensory stimulation

◦ Most often auditory and visual

✦ Hearing thoughts spoken by another voice

✦ Voices arguing or commenting on behavior

◦ People who have auditory hallucinations may misattribute their own voice as someone

else’s voice

• NEGATIVE SYMPTOMS

◦ Behavioral deficits in motivation, pleasure, social closeness, and emotion expression

◦ Endure beyond an acute episode

◦ Have profound effects on the lives of people with Schizophrenia; Strong predictory of a

poor quality of life

◦ Representing two domains:

✦ Motivation and pleasure domain - motivation, emotional experience, sociality

✦ Expression domain: outward expression of emotion, vocalization

• 5 TYPES OF NEGATIVE SYMPTOMS:

◦ Avolition - Lack of motivation; apathy

◦ Asociality - Little interest in being around others and close relationships

◦ Anhedonia - Inability to experience pleasure

✦ Consummatory pleasure - refers to the amount of pleasure experienced in the

moment or in the presence of something pleasurable

✦ Anticipatory pleasure - refers to the amount of expected or anticipated pleasure from

future events or activities

✦ Schizophrenia appears affect anticipatory pleasure, not consummatory pleasure

◦ Blunted affect - Lack of outward expression of emotion

◦ Alogia - Significant reduction in speech

• DISORGANIZED SYMPTOMS

◦ Disorganized speech (formal thought disorder)

✦ Problems in organizing ideas and in speaking coherently

✦ Loose associations (derailment)

✧ Difficulty sticking to one topic

◦ Disorganized behavior

✦ Difficulty organizing behaviors and conforming to community standards

✦ Catatonia

✧ Peculiar, increased, repeated gestures or immobility

✧ Seldom seen today due to effective medications

In the DSM-5:

• Two or more of the following symptoms for at least 1 month; one symptom should be

either 1, 2, or 3:

◦ 1. Delusions

◦ 2. Hallucinations

◦ 3. Disorganized speech

◦ 4. Disorganized (catatonic) behavior

◦ 5. Negative symptoms (diminished motivation or emotional expression)

• Functioning in work, relationships, or self-care has declined since onset

• Signs of disorder for at least 6 months; or if during a prodromal or residual phase,

negative symptoms or two or more of symptoms 1-4 in less severe form

Other Schizophrenia Spectrum Disorders

• Schizophreniform Disorder

◦ Same symptoms as schizophrenia

◦ Symptom duration greater than 1 month but less than 6 months

• Brief Psychotic Disorder

◦ Lasts one day to one month

◦ Symptoms often brought on by extreme stress, such as bereavement

• Schizoaffective Disorder

◦ Symptoms of both schizophrenia and mood disorders

• Delusional Disorder

◦ Persistent delusions

✦ grandiose delusions, delusions of erotomania (believing that one is loved by some

other person, usually a complete stranger with a higher social status), and somatic

delusions (delusions about body functions)

• Attenuated Psychosis Syndrome (APS)

◦ A condition where someone has psychotic symptoms that are not sever enough to be

diagnosed as a psychotic disorder

◦ Prodrome/prodromal - refers to early signs of the disease

Etiology of Schizophrenia

BEHAVIORAL GENETICS RESEARCH

• Genetically heterongeneous

◦ Genetic factors may vary from case to case

• Family studies

◦ Relatives at increased risk

◦ Risk increases as genetic relationship becomes closer

◦ Negative symptoms have stronger genetic component

◦ Incidenc highest among children with both parents with a schizophrenia or bipolar

disorder diagnosis

✦ Suggests some shared genetic vulnerability

◦ The role of environment cannot be discounted

• Twin studies

◦ 44% risk for MZ twins vs 12% risk for DZ twins

◦ Negative symptoms have stronger genetic component

◦ Children of MZ twin without schizophrenia were more likely to develop schizophrenia

(94.% vs 1% in general population)

• Adoption studies

◦ Children born to women with schizophrenia raised by adoptive parents without

schizophrenia

◦ Increased likelihood of developing schizophrenia

• Familial high-risk studies

◦ Longitudinal study — follows offspring of parents with disorders

◦ Risk of developing schizophrenia is highest for offspring of a parents with schizophrenia

MOLECULAR GENETICS RESEARCH

• Observed mutations are rare:

◦ CNVs account for less than 1% of genetic variance

◦ SNPs account for less than 25% of genetic variance

• Only some people with these rare mutations have schizophrenia

• Findings confirms genetic heterogeneity of schizophrenia

◦ People with the same disorder may not have the same genetic factors

NEUROTRANSMITTERS

• Dopamine Theory

◦ Disorder due to excess levels of dopamine

✦ Drugs that alleviate symptoms reduce dopamine activity

✦ Amphetamines, which increase dopamine levels, can induce a psychosis

◦ Theory revised

✦ Excess dopamine receptors related mainly to positive and disorganization symptoms

✦ Negative symptoms may be more clearly accounted for by other neurotransmitters

✦ Disconnect between behavioral and pharmacological effects

• Other Neurotransmitters

◦ Serotonin

✦ New drugs partially block D2 receptor AND block serotonin receptor 5HT2

✦ Regulate dopamine neurons in mesolimbic pathway

◦ Glutamate

✦ NMDA receptor part of the glutamate system

✧ Decreased NMDA receptor activity and lower levels of glutamate

✧ Also associated with cognitive defecits and disorganization

BRAIN STRUCTURE AND FUNCTION

• Enlarge Ventricles

◦ Implies loss of brain cells

◦ Correlated with:

✦ Poor performance on neuropsychological tests

✦ Poor functioning prior to onset of disorder

✦ Poor response to medication treatment

◦ Not specific to schizophrenia

• Factors Involving Prefrontal Cortex

◦ Plays a role in speech, decision making, emotion, goal-directed behavior

◦ Reduction in gray matter and overall volume

✦ Antipsychotic may contribute to loss

◦ Poorer performance on neuropsychological tests designed to tap into functions of

prefrontal region

◦ Lower glucose metabolism when performing neuropsychological tests

◦ Less activation associated with more severe negative symptoms

• Temporal Cortex and Surrounding Regions

◦ Structural and functional abnormalities in the temporal cortex

✦ Temporal gyrus, hippocampus, parts of the insula, fusiform gyrus, amygdala, cingulate

cortex

◦ Reduced hippocampal volume

✦ Twins with schizophrenia

✦ During first episode of schizophrenia

✦ Relatives of people with schizophrenia

✦ Related to stress reactivity and a disrupted HPA axis

• Connectivity in the Brain

◦ Less connectivity in brain white matter in frontal and temporal cortices

✦ Associated with genetic diathesis for schizophrenia

◦ Less connectivity between brain networks

✦ Frontopareital and default-mode networks

✦ Also found in healthy relatives of people with schizophrenia

◦ Helpful for predicting who will respond well to antipsychotic medication treatment

• Early Environmental Factors

◦ Damage during gestation or birth

✦ High rates of delivery complications

✧ May result in reduced oxygen and loss of cortical gray matter

✦ Increased risk for those with a genetic diathesis

◦ Maternal infection

✦ Presence of toxoplasma gondii associated with 2.5x greater risk

• Brain Development Factors

◦ Developmental factors

✦ Prefrontal cortex matures in adolescence or early adulthood

✦ Dopamine activity also peaks in adolescence

✦ Adolescence is a time fraught with stress

✦ Excessive pruning of synpatic connections

✦ Use of cannabis during adolescence associated with increased risk

◦ May explain why symptoms appear in late adolescence but brain abnormalities occur

early in life

• Psychological Factors

◦ Greater vulnerability to stress

✦ Individuals with schizophrenia and their first-degree relatives more reactive to stress

✧ Greater decreases in positive mood and increases in negative mood

◦ Sociocultural factors

✦ Poverty — higher rates among urban poor

✦ Urbanicity — Higher rates among people living (born and raised) in urban areas

✧ Nearly 3 times as high in urban than rural areas

✦ Migration — first and second generation migrants

• Family Factors

◦ Schizophrenic mother

✦ Cold, domineering, conflict-inducing parent causes schizophrenia

✦ No support for this theory

◦ Family relationships do not cause schizophrenia, but may influence course of the illness

✦ e.g., unclear communication, high levels of conflict

✦ Plausible that these factors are a response to having a family memory with

schizophrenia

• Families and Relapse

◦ Family environment imapcts rrelapse

◦ Expressed Emotion (EE)

✦ Hostility, critical comments, emotional overinvolvement

✦ Associated with greater relapse

✦ Cultural differences in the impact of EE

◦ Bidirectional association

✦ Expression of unusual thoughts by person with schizophrenia —> Increase critical

comments by family

✦ Critical comments by family —> Increase unusual thoughts by person with

schizophrenia

RETROSPECTIVE DEVELOPMENTAL STUDIES

• Developmental hisotries of children who later developed schizophrenia

◦ Lower IQ

◦ More often delinquent, withdrawn, disagreeable (boys), passive (girls)

• Coding of home movies

◦ Poorer motor skills

◦ More expression of negative emotion

PROSPECTIVE DEVELOPMENTAL STUDIES

• New Zealand study: Lower IQ scores predicted onset

• Australian study: Clinical-high-risk study —> Examines people with early symptoms;

Reduced gray matter volume onset of schizophrenia

• North American Prodrome Longitudinal Study

◦ Identified factors associated with the development of psychosis

✦ Having a biological relative with schiz; Recent decline in functioning; High levels of

positive symtpoms, social impairment

High levels of impaired cognitive functioning

Treatments

MEDICATIONS

• First-Generation Antipsychotics

◦ Reduce positive and disorganization symptoms

◦ Little or no effect on the negative symptoms

◦ 30% of people don’t respond

✦ Many stop quit due to side effects

◦ Maintenance dosages help to prevent relapse

◦ Side effects:

✦ Sedations, dizziness, restlessness, sexual dysfunction

✦ Extrapyramidal side effects (e.g., tremors, shuffling gait)

✦ Tardive dyskinesia

• Second-Generation Antipsychotics

◦ Equally as effective as first-generation at reducing positive symptoms and

disorganization

✦ Modestly more effective at reducing negative symptoms

✦ More effective at improving cognitive functioning

◦ Also produce unpleasant side effects: Weight gain

✦ Associated with other serious health concerns (e.g., Type 2 Diabetes)

✦ Many people also stop taking these medications

• Evaluation of Drug Treatments

◦ A review of over 60 years of clinical trials:

✦ Just over half of people with schizophrenia had a minimal response compared to

placebo

✦ Only 23% had a good response

◦ Even though these drugs work better than placebo, they do not work well for many

people

◦ More work is needed to develop better medications for schizophrenia

PSYCHOLOGICAL TREAMENTS

• Patient Outcomes Research Team (PORT) Treatment recommendation:

◦ Medication plus psychosocial intervention

◦ Social skills training, cognitive behavior therapy, and family-based treatments

◦ ^ Combined treatment is associated with:

✦ Lower rates of relapse and treatment discontinuation

✦ Greater improvements in functioning

• Social Skills Training

◦ Teach skills for managing interpersonal situations

✦ Completing a job application

✦ Reading bus schedules

✦ Make appointments

◦ Involves role-playing and other practice exercises, both in group and in vivo

◦ Associated with fewer relapses, better social functioning, and a higher quality of life

• Family Therapy

◦ Goal: reduce expressed emotion

◦ Components common across family therapies for schizophrenia:

✦ Education about schizophrenia

✦ Information about antipsychotic medications

✦ Blame avoidance and reduction

✦ Communication and problem-solving skills within family

✦ Social network expansion

✦ Instilling hope

◦ Cognitive Behavioral Therapy (CBT)

✦ Recognize and challenge delusional beliefs

✦ Reduces negative symptoms

✧ Challenges belief structures tied to low expectations forr success and pleasure;

Currently most effective treatment

✦ Cognitive-behavioral social skills training (CBSST)

✧ Combines social skills training and cognitive behavioral therapy; Focuses on

rreducing symptoms and improving functioning

✦ The earlier treatment begins the better

• Other Psychological Treatments

◦ Cognitive remediation or cognitive training

✦ Include hours of computer-based training in attention, memory, and problem solving

◦ Psychoeducation

✦ Educate people about their illness

✦ Effective in reducing relapse and rehospitalization and increasing medication

compliance

◦ Residential treatment

✦ Vocal rehabilitation

✦ Residents learn marketable skills thereby increasing community functioning

✦ Cognitive remediation or cognitive training

✦ Include hours of computer-based training in attention, memory, and problem solving