PSC 168: Abnormal Psychology Midterm 3

CHAPTER 9 Schizophrenia

History of Schizophrenia

Emil Kraepelin

* Coined the term “dementia praecox” (1898
* Meaning premature dementia – early onset, progressive
* Believed it to be a cognitive disorder, not a mood disorder
* Viewed schizophrenia as something that couldn’t be recovered from

Eugen Bleular

* Broke with Kraepelin’s description – did not believe early onset or progressiv
* Introduced the term “schizophrenia” (1908
* Meaning? “Split mind
* Really referring to the split between the patient’s thoughts and reality

Schizophrenia Myths

* not multiple personalities
* link with violence is not evident
* Theory of schizophrenic mother is not true

Schizophrenia diagnosis

* characterized by disordered thinking, in which ideas are not logically related; faulty perception and attention; a lack of emotional expressiveness; and disturbances in behavior, such as a disheveled appearance.

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For a diagnosis of schizophrenia, a person has to have at least **two symptoms**, and o**ne of these should be delusions, hallucinations, or disorganized speech:**

* delusions
* hallucinations
* disorganized speech
* disorganized (or catatonic) behavior
* negative symptoms (diminished motivation or emotional expression)\]

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Schizophrenia symptoms are often described in three broad domains: positive, negative, and disorganized

Schizophrenia prevalence and diagnosis

* lifetime prevalence of schizophrenia is around 1%
* affects men slightly more often than women

Schizophrenia Positive, Negative and disorganized Symptoms

* **Positive symptoms**: excesses and distortions and include hallucinations and delusions. Also referred to as psychotic symptoms.
* Examples: Grandeur, Reference, Thought broadcasting, Persecutory
* **Delusions**: beliefs contrary to reality and firmly held despite dis-confirming evidence, common positive symptoms
* **Hallucinations**: sensory experiences in the absence of any relevant stimulation from the environment. More often auditory (Hearing thoughts spoken by another voice or voices arguing or commenting on behavior)
* greater activity in Broca’sarea
* a report hearing voices- problem in the connections between the frontal lobe areas that enable the production of speech and the temporal lobe areas that enable the understanding of speech
* **Negative Symptoms**: deficit symptoms
* deficits in motivation, pleasure, social closeness, and emotion expression.
* Avolition (Apathy), Asociality, anhedonia, Blunted Affect- refers to a lack of outward expression of emotion, Alogia - refers to a significant reduction in the amount of speech.
* **Disorganized Symptoms**: disorganized speech and behavior - cognitive symptoms

DSM-5 criteria of Schizophrenia

**At least 2 of the following symptoms**, at least one of which is **delusions, hallucinations,** or **disorganized speech**

* Delusions
* Hallucinations
* Disorganized speech
* Disorganized (or catatonic) behavior
* Negative symptoms (diminished motivation or emotional expression
* Symptoms must last for at least 6 months

Positive symptoms: Delusions

* **Beliefs contrary to reality** (eg. I’m the president)
* **Firmly held despite evidence to the contrary**
* Tend to be highly unlikely
* Example
* Grandeur
* Reference - belief that messages are for you
* Thought broadcasting - think thoughts can be heard by others
* Persecutory - someone close to them is being mistreated or going to harm them

Positive symptoms: Hallucinations

**Sensory experiences** in the absence of sensory stimulation

* Person can see, smell, hear, taste, or feel something that isn’t there

Most often auditory and visual, e.g.:

* Hearing thoughts spoken by another voice
* Voices arguing or commenting on behavior

Negative symptoms

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

* **Strong predictor of poor quality of life**
* Two domains
* **Motivation and pleasure**: Motivation, emotional experience, sociality
* **Expression**: Outward expression of emotion, vocalization

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**Motivation domain**

* Avolition: Diminished motivation; apathy
* Asociality: Little interest in being around others and having close relationships
* Anhendonia: Inability to experience pleasure
* People with schizophrenia have **more difficulty with anticipating pleasure** rather than experiencing pleasure (consummatory pleasure)

**Expressive domain**

* Blunted affect: Lack of outward expression of emotion, inner emotional experience is often not affected
* Alogia: Significant reduction in amount of speech

Disorganized symptoms

Disorganized **speech** (formal thought disorder)

* Problems in organizing ideas and in speaking coherently
* Loose associations (derailment)
* Difficulty sticking to one topic \n

Disorganized **behavior**

* Difficulty organizing behaviors and conforming to community standards (i.e., wandering, dressing oddly, collecting garbage)
* **Catatonia**: Peculiar, increased, repeated gestures or immobility
* Seldom seen today due to effective medications

Facts and stats on Schizophrenia

* Top 10 leading cause of disability worldwide
* \~1% of the population
* Affects men slightly more often than women
* Typical age of onset 18-25; later for women
* Often experience several acute episodes with less severe symptoms between episodes
* Diagnosed more frequently among Black men – historical roots, bias among clinicians
* Elevated rates of suicide, substance use

The Protest Psychosis

* Identified trend of Ionia State Hospital to diagnose African Americans with schizophrenia in the 1960s because of their civil rights ideas (“protest psychosis”)
* Suggests sudden influx of such diagnoses could be traced to a change in wording in the DSM-II, which added “hostility” and “aggression” as signs of schizophrenia
* Wording was not racist per se, but effects were
* Unintentionally reflected social tensions of 1960s, influencing link between protest and mental illness
* Argument that this change resulted in structural racism
* Biases are historically “...structured into clinical interactions before doctors or patients enter examinations rooms” (p. xi) and are “embedded into the very DNA of healthcare delivery systems” (p. 202)
* Facility was transformed into prison in 1980s

Other Schizophrenia Spectrum Disorders

* **Schizophreniform disorder**: symptoms are the same as those of schizophrenia but last only 1 to 6 months.
* **Brief psychotic disorder**: lasts from 1 day to 1 month and is often brought on by extreme stress, such as bereavement.
* **Schizoaffective disorder:** symptoms of both schizophrenia and mood disorders
* Must have either a depressive and/or \n manic episode(s)
* *Psychotic symptoms must be independent of mood episodes*
* **Delusional Disorder:** Persistent delusions lasting at least 1 month
* No other psychotic symptoms

Etiology of Schizophrenia

Genetic Influences

* **heritability estimate for schizophrenia is 0.77**
* Higher concordance in MZ (45%) vs DZ (12%) twins
* Genetically heterogeneous –varies from person to person
* Overlapping genetic risk factors with other diagnoses (e.g., bipolar, autism, ID)

Behavior Genetics Research

* findings suggest that there may be some shared genetic vulnerability between schizophrenia and bipolar disorder
* Approximately 25 candidate genes have been identified for schizophrenia over the years

The Role of Neurotransmitters

* Theory that schizophrenia is related to excess activity of the neurotransmitter dopamine is based principally on the knowledge that drugs effective in treating schizophrenia reduce dopamine activity.
* Low levels of glutamate have been found in the cerebrospinal fluid of people with schizophrenia, and postmortem studies have revealed low levels of the enzyme needed to produce glutamate

Brain Structure and Function

* enlargement of the ventricles and dysfunction in the prefrontal cortex and temporal cortex
* problems in how different areas of the brain are connected
* reductions in gray matter and overall volume (size) in the prefrontal cortex
* volume of the hippocampus was significantly reduced

Psychological Influences

* appear to be very reactive to the stressors we all encounter in daily living.

Sociocultural Factors

* poverty (socioeconomic status), trauma, urbanicity (living in cities), and migration (moving from one country to another) each appears to be independently associated with a higher risk of developing schizophrenia.

Developmental Factors

* adults with schizophrenia scored lower on IQ and other cognitive tests
* social and academic difficulties in childhood predicted conversion to a psychotic disorder

Etiology: Neurobiological factors in Schizophrenia

* Neurotransmitters: Dopamine hypothesis
* Theory that schizophrenia is related to excess activity of the neurotransmitter dopamine is based principally on the knowledge that drugs effective in treating schizophrenia reduce dopamine activity.


* Brain structure
* Ventricles – enlarged
* Reduced gray matter/volume (frontal and temporal regions, basal ganglia, hippocampus, amygdala
* Brain function – reduced activation
* Prefrontal
* Limbic
* Basal ganglia
* Hippocampus
* Connectivity
* Stress reactivity?
* Diminished connectivity between brain regions

Etiology: Environmental factors in Schizophrenia

Complications during pregnancy or birth

* Maternal infection during pregnancy
* Risk factors x genetic vulnerability → changes in brain development → symptom onset in adolescence/early adulthood
* PFC and pruning?
* Pubertal changes → HPA axis/cortisol → DA activity?
* What about marijuana?
* For people who have schizophrenia already, use is associated with worsening symptoms
* Emerging research suggesting can be a trigger in adolescence particularly among those who are vulnerable to schizophrenia

Etiology: Sociocultural factors and Family factors Schizophrenia

* Poverty: Higher rates among urban poor


* Trauma: Child trauma or maltreatment a risk factor for nearly all psychological disorders, including schizophrenia
* Urbanicity: Higher rates (\~3x) among people living in urban areas
* Migration: First- and second-generation migrants
* What’s the link?

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Family relationships do not cause schizophrenia, but may influence course

* Expressed emotion (EE)
* Hostility, critical comments, emotional overinvolvement
* Associated with greater relapse
* Bidirectional
* Expression of unusual thoughts by person with schizophrenia → increase critical comments by family
* Critical comments by family → increase unusual thoughts by person with schizophrenia

Treatment of Schizophrenia

Medications

* antipsychotic drugs- people who respond positively to the antipsychotics are typically kept on so-called maintenance doses of the drug, just enough to continue the therapeutic effect.
* Act on dopamine system, also with impacts on serotonin, norepinephrine
* **Treat positive symptoms**


* side effects: sedation, dizziness, blurred vision, restlessness, and sexual dysfunction. Extrapyramidal side effects, resemble the symptoms of Parkinson’s disease. People taking antipsychotics may develop tremors of the fingers, a shuffling gait, and drooling
* **Medications are not very effective for negative symptoms**
* Other medications sometimes used (SSRIs, mood stabilizers)

Psychological Treatments

* Cognitive Behavioral Therapy: Challenge delusions/hallucinations, motivational enhancement
* Family Therapy: High familial stress may precede diagnosis and relate to maintenance of symptoms
* Social Skills Training: Teaching how to navigate interpersonal situations, how to discuss medications with doctors, fill out job apps, interview for jobs, read bus schedules, initiate/maintain conversations

For a diagnosis of schizophrenia, what symptom(s) must be present?

What distinguishes a delusion from a hallucination?

What neurotransmitter has been commonly associated with schizophrenia?

CHAPTER 8 Dissociative Disorders and Somatic Symptom and Related Disorders

Dissociative Disorders

There are 3 dissociative disorders...

* Depersonalization/derealization disorder
* Dissociative amnesia
* Dissociative identity disorder \n

In general, they involve...

* Severe alterations or detachments
* Affect identity, memory, and/or consciousness
* Severe form of normal perceptual experiences

What is “dissociation”?

Dissociation

* Some aspect of emotion, memory, or experience being inaccessible consciously
* Some types of dissociation 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

DSM-5 Criteria

* **Depersonalization OR derealization**
* Depersonalization: Experiences of detachment from one’s mental processes or body, as though one is in a dream
* Derealization: Experiences of unreality of surroundings
* Symptoms are persistent or recurrent
* Realty testing remains intact
* Symptoms are not explained by substances or another dissociative, psychological, or medical disorder

Depersonalization/derealization disorder

* Prevalence around 0.8(?)


* Symptoms are usually triggered by stress
* May be related to difficulties integrating sensory and somatic information
* Childhood trauma is often reported
* Usually begins in adolescence
* Frequently comorbid with other disorders
* Personality disorders
* Depression or anxiety disorders (90%)

Clinical Descriptions of the Dissociative Disorders

* The DSM-5 includes three major dissociative disorders: depersonalization/derealization disorder, dissociative amnesia, and dissociative identity disorder
* Depersonalization/derealization disorder Experience of detachment from the self and reality
* Depersonalization is a sense of being detached from one’s self
* disorder involves no disturbance of memory.
* symptoms usually triggered by stress.
* Dissociative amnesia Lack of conscious access to memory, typically of a stressful experience. The fugue subtype involves traveling or wandering coupled with loss of memory of one’s identity or past.
* the memory loss of amnesia typically involves information about a traumatic event or events, but Procedural memory remains intact
* In the fugue subtype person typically disappears from home and work but don’t remember the events that took place during the fugue.
* Dissociative identity disorder At least two distinct personality states that act independently of each other
* person experiences at least two separate personality states or experiences of possession
* Recurrent gaps in memory for events or important personal information that are beyond ordinary forgetting

Dissociative amnesia

DSM-5 Criteria

* Inability to remember important autobiographical information, usually of a traumatic stressful nature, that is too extensive to be ordinary forgetfulness
* Amnesia is not explained by substances or other medical/psychological conditions
* Specify dissociative fugue sub-type if the amnesia is associated with bewildered and apparently purposeful wandering
* May last several hours to several years
* Usually disappears as suddenly as it began, with complete recovery of memory
* Most people with intense traumatic experiences do not experience dissociative amnesia

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Important to 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
* **Prevalence around 1.8%(?)**

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 during the fugue

Dissociative identity disorder (DID) DSM-5 Criteria

* Disruptions of identity characterized by 2+ distinct personality states or experience of “possession”


* Disruptions lead to discontinuities in sense of self or agency, as reflected by altered cognition, behavior, affect, perceptions, consciousness, memories, or sensory-motor functioning.
* May be observed by others or reported by patient


* Recurrent gaps in memory for events or important personal information that are beyond ordinary 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 imaginary playmate or fantasy play

Unique aspects of DID

Alters: The different identities

* 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
* Primary alter may have no memory of what other alters do
* The individual may not necessarily perceive these as separate personalities, but rather as dramatic shifts in their sense of self and agency and recurrent periods of amnesia

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* Host: The identity that keeps other identities together


* Switch: Quick transition from one personality to another

DID facts and stats

* 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
* More common in women than men (9:1)
* Average number of identities is close to 15
* High comorbidity rates, with a lifelong chronic course
* **Prevalence 1.5%(?)**

Dissociative disorders etiology: \n DID specifically

* The diagnostic criteria and growing literature may have increased detection and recognition of symptoms.
* brain regions that are involved in processing bodily cues related to emotion experience, such as the anterior cingulate cortex, appear to be underactive when viewing emotionally evocative images

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Posttraumatic model

* Most have histories of horrible, unspeakable, child abuse
* Mechanism to cope with/escape from impact of trauma?
* Mixed findings about whether childhood abuse predicts tendencies for adults to dissociate

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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
* Reinforcement of identified alters and suggestive techniques might promote symptoms in vulnerable people
* Not viewed as conscious deception
* There is some evidence in support of this 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
* Rapid increase in the number of alters as treatment progresses
* Alters share memories, even when they report amnesia
* Implicit memories are transferred between alters

Dissociative disorders etiology: In general

Little is known about the etiology

* No identified reports of DID or dissociative amnesia before 1800s
* Increased rates since 1970s
* Appearance of DID in popular culture
* DSM-III (1980) defined DID for the first time

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

Brain mechanisms related to depersonalization/ derealization

* May have difficulties in way the brain integrates information from different sensory/bodily sources
* Can induce brief symptoms in people who do not have diagnosis by providing mismatched/unexpected sensory experiences
* Maybe brain differences in areas related to processing bodily cues related to emotion?

Treatment of Dissociative Disorders

No well-validated treatments available

* No randomized controlled trials
* Medications don’t help

Main goal:

* The goal of treatment should be to convince the person that splitting into different personalities is no longer necessary to deal with traumas
* Teach person more effective ways to cope with stress and regulation emotions
* Psychoeducation to identify triggers

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* Psychodynamic treatment is probably used more for DID and the other dissociative disorders than for any other psychological disorder. The goal of this treatment is to overcome repressions

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Psychodynamic approaches

* DID is believed to arise from traumatic events that the person is trying to block from consciousness \n (repress)
* 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 & related disorders

Excessive concerns about physical symptoms or health:

* Tendency to seek frequent medical treatment
* Often see several physicians for a given health concern
* May try many different medications
* Hospitalization and surgery are common experiences

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* Distress over symptoms is authentic
* Criticisms of diagnostic criteria
* Conditions are remarkably varied
* Patients often find these diagnoses stigmatizing
* Tend to co-occur with anxiety disorders, mood disorders, and personality disorders

Clinical Description of Somatic Symptom and Related Disorders

* three major disorders in this category: somatic symptom disorder, illness anxiety disorder, and conversion disorder.
* Specify if predominant pain

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

* **Excessive thought, distress, and behavior related to somatic symptom(s) or health concerns**, as indicated by at least one of the following:


1. health-related anxiety
2. disproportionate and persistent concerns about the
seriousness of symptoms
3. excessive time and energy devoted to health concerns
4. symptoms present for 6 months

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* Distress revolves around a somatic symptom that exists


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

Somatic symptom & related disorders

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 those symptoms

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Factitious disorder

* Falsification of psychological or physical symptoms, without evidence of gains from those symptoms

Illness anxiety disorder

DSM-5 criteria

* 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 care)
* 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 in the community
* Fears are not easily calmed
* May become frustrated when attempts to soothe worries fail

Conversion disorder

DSM-5 criteria

* One or more symptoms affecting voluntary motor or sensory function
* The symptoms are incompatible with recognized medical disorder
* Symptoms cause significant distress or functional impairment or warrant medical evaluation \n

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

Conversion disorder facts and stats

* 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 usually rapid
* Prevalence less than 1%
* More common in women than men
* Highly likely to meet criteria for another somatic symptom disorder

Malingering & factitious disorder

Malingering

* Person intentionally fakes symptoms to avoid a responsibility or to achieve some reward

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Factitious disorder

* Formerly “Munchausen Syndrome”•DSM-5 Criteria
* Fabrication or induction of physical or psychological symptoms, injury, or disease
* Deceptive behavior is present in the absence of obvious external rewards
* Can be:
* Imposed on self—presents self as ill, impaired or injured
* Imposed on another—makes other ill, impaired, or injured

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Risk factors

* Childhood traumas
* Parents/caretakers who were emotionally unavailable due to illness or emotional problems
* Serious illness as a child
* Failed aspirations to work in the medical field
* Low self-esteem

What causes somatic symptom disorders

NOT heritable (though “health anxiety” moderately so)

* Little known about etiology of the DSM-5 somatic symptom-related disorders
* Most research used 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

Etiology of Somatic Symptom and Related Disorders

Neurobiological Factors

* Heightened activity in brain regions activated by:
* Unpleasant body sensations (anterior insula and anterior cingulate cortex)
* Processing bodily sensations (somatosensory cortex)
* Heightened activity in these regions is related to greater propensity for somatic symptoms
* the person believes that the symptoms are a sign of an underlying long-term disease

What causes somatic symptom disorders?

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

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Behavioral factors

* 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

What causes conversion disorder?

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 factors shape how conversion symptoms unfold

* Modeling (mass hysteria)
* More common among people
* From rural areas
* From lower resourced backgrounds (SES)

Treatment of Somatic Symptom and Related Disorders

There are challenges...

* 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

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* health care system intervention involves alerting physicians when a patient is an intensive user of health care services so as to minimize the use of diagnostic tests and medications
* Often starts with 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 behavior therapy (CBT): (1) identify and change the emotions that trigger somatic concerns, (2) change cognitions regarding their somatic symptoms, and (3) change behaviors so as to improve social interactions
* do more to reduce the distress about somatic symptoms than they do to reduce the actual somatic symptoms

Treatment of somatic symptom disorders

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 can help patients disengage from a focus on their symptoms
* Internet-based approaches may also be helpful with brief clinician guidance

More effective in reducing health concerns, depression, anxiety than standard medical care or psychodynamic treatment of somatic symptom disorders

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Research on conversion disorder treatment

* 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

What do dissociative and somatic symptom disorders have in common

both triggered by stressful experiences but don’t have direct outward expression of anxiety

What are the 2 primary models of DID?

* post traumatic - a mechanism to deal with stress and trauma


* sociocognitive model - maybe people seek explanations for trauma, and alters may appear as suggestions from therapists

What might be a cognitive-behavioral explanation of somatic symptom disorders?

people are more likely to pay attention to their bodies and physical sensations and attuned to physicals health cues then interpret them in ways not typical and overreact of their symptoms that lead to anxiety.

CHAPTER 11 Eating Disorders

page 600

What’s in common with Eating Disorders

* All involve disruptions in eating behavior
* Many involve extreme fear and apprehension about weight gain

Anorexia nervosa (AN) DSM-5 criteria

* **Restriction of energy intake** relative to requirements leading to a **significantly low body weight** in the context of age, sex, developmental trajectory, and physical health (e.g., 10-15% below expected BMI)
* **Intense fear** of gaining weight or becoming fat, even though underweight.
* Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or denial of the seriousness of the current low body weight — i.e., **distorted body image** or sense of body shape

Anorexia nervosa types

* **Restricting type**: Weight loss is achieved by severely limiting food intake **(no purging)**
* **Binging/Purging type**: The person has also regularly \n engaged in binge eating and purging
* i.e., Behavior like bulimia nervosa (BN), but meets weight criteria for AN
* Longitudinal research suggests limited validity of subtypes, but maybe some clinical utility

Anorexia nervosa Defining Features

“Successful” weight loss

* 10-15% below expected body weight
* Severe calorie restriction to the point of semi-starvation
* May also engage in some purging/excessive exercise
* Relentless pursuit of thinness
* Often begins with simple dieting and escalates

Associated Features

* Weight loss methods have life threatening consequences
* Can result in cessation of menstrual cycle, growth of body hair, dry skin, electrolyte imbalances, heart/kidney failure
* Denial of problem
* Severity ratings are based on BMI

Anorexia nervosa facts/stats

* Effects

Anorexia nervosa treatment

Often chronic without treatment (50-70% recover/improve—can take \~6-7 years)

* #1 goal: Increase weight, avoid medical complications and death — often involves medical-based interventions and hospitalization
* #2 goal: Long-term maintenance of weight gain
* CBT: Focuses on restoring weight, correcting dysfunctional attitudes about eating, body shape, \n weight
* Results in improvements in symptoms \~1 yr later
* Also family-based therapy

Bulimia nervosa DSM-5 criteria

* **Binge eating**—the core feature of bulimia
* Binge = Eating excessive amounts of food (e.g., 2 days worth of food at a single sitting)
* Eating is perceived as uncontrollable
* Often in “secret”, often during times of stress
* 1x/per week for at least 3 months


* **Compensatory behaviors**—doing something to “get rid” of the calories
* Purging = Self-induced vomiting, diuretics, laxatives
* Excessive exercise
* Fasting (\~1/3 do this)
* 1x/per week for at least 3 months


* Body shape and weight are extremely important to self-evaluation


* Disturbance is not due to AN (i.e., not severely under weight)

Bulimia nervosa associated features

Medical features

* Most within >10% of a “normal” weight (i.e., BMI), many actually overweight
* Purging can result in severe medical problems
* Erosion of dental enamel, swollen salivary glands, electrolyte imbalances, kidney failure, cardiac arrhythmia, seizures, intestine and colon dysfunction due to excessive laxative use

Psychological features

* Overly concerned with body shape
* Fear of gaining weight
* Fear of losing control

Bulimia nervosa facts/stats

* BN affects 1-2% of women


* 90% are women
* Exists across cultures, but like AN, mostly Westernized, developed
* Onset typically in late adolescence/early adulthood
* Often chronic without treatment, but may wax and wane (10-20% remain symptomatic)
* **Commonly co-occurs with depression, personality disorders, anxiety disorders, substance use, conduct disorder**
* Suicide rates are higher than among healthy individuals, but lower than AN

Bulimia nervosa treatment

* CBT is the best-validated and most current standard for treatment
* Challenge societal standards for physical attractiveness
* Challenge beliefs about weight and dieting
* Challenge all-or-nothing beliefs about food (e.g., One bite of high-calorie food does not need to trigger a binge)
* Increase self-assertiveness skills
* Increase regular eating patterns (three meals per day)
* 68—75% recover, but \~10—20% remain fully symptomatic
* Intervening soon after diagnosis is made linked with better prognosis
* CBT more effective than medication but adding medication may help alleviate depression

What is the key distinction between AN and BN?

WEIGHT LOSS.

* AN – lose lots of weight
* BN – don’t lose lots of weight

Binge Eating Disorder (BED) DSM-5 criteria

Recurrent episodes of binge eating, characterized by both of the following:

* Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food that is definitely larger than most people would eat in a similar period of time under similar circumstances
* Lack of control over eating during the episode

Binge-eating episodes associated with 3+ of the following:

* Eating much more rapidly than normal
* Eating until feeling uncomfortably full
* Eating large amounts of food when not physically hungry
* Eating alone because of feeling embarrassed by how much one is eating
* Feeling disgusted with oneself, depressed, or very guilty afterwards

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* Marked distress regarding binge eating is present
* Binge eating occurs at least 1x/week for 3 months
* **Not** **associated with recurrent use of inappropriate compensatory behavior (e.g., purging)** and does **not** occur exclusively during the course Anorexia Nervosa, Bulimia Nervosa

BED associated features

* Most fall into the “obese” weight range (BMI > 30; 2-25% of people with obesity)
* Health consequences: Type II diabetes, cardiovascular disease, sleep problems
* BUT... not all people who are in the “obese” weight range have BED
* Often older than those with BN or AN
* Often have history of dieting
* Tend to have comorbid diagnoses (more so than people with obesity who do not binge)
* Concerned about weight and shape

BED facts/stats

* Affects 0.2-4.7% of the general population
* More common in females
* Appears cross culturally, but again, more Westernized, developed
* Onset usually in adulthood
* Often chronic (average duration is about 14 years)
* Commonly comorbid with mood disorders, anxiety disorders, ADHD, conduct disorder, substance use

BED treatment

* Mostly CBT based
* Targets binge eating through self-monitoring, self-control, and problem-solving skills
* More effective than medication
* CBT (whether individual with therapist or guided self-help CBT) more effective than behavioral weight-loss programs
* 25-82% of people with BED recover

Etiology: Genetics

Heritability

* AN: 0.48-0.74
* BN: 0.26-0.55
* Key features of eating disorders, body dissatisfaction, desire for thinness, binge eating, and weight preoccupation, are heritable

Eating disorders run in families

* Higher concordance rates for MZ than DZ twins for AN and BN
* First-degree relatives more likely to have the disorder – 10x for AN, 4x for BN
* Relatives of people with BED+obesity more likely to have BED themselves (20%) than relatives of people who are obese but don’t have BED (9%)

Hard to identify specific genes since eating disorders relatively rare

Etiology: Neurobiological factors

Hypothalamus → cortisol?

* Regulates hunger/eating, stress hormones like cortisol
* Hormone changes probably a result of self-starvation rather than causal of disorder

Brain regions involving habit and reward

* View food images or deliver “tastes” while in scanner
* Dorsal striatum activation – involved in habitual choices and anxiety
* Greater activation in regions of brain associated with DA/reward when presented with food cues → cravings → increased likelihood of gaining weight (BED/obesity?)

Neurotransmitters

* Serotonin – eating/satiety
* Low levels of serotonin metabolites among people with AN and BN – reduced serotonin activity?
* Antidepressants that increase serotonin often effective in treatment of eating disorders (but could be linked \n to comorbid depression?)
* Dopamine – reward (liking/wanting/craving food)
* Changes probably consequence of AN, not cause

\
* BUT... these things do not account for body image disturbances, fear of gaining weight

Etiology: Cognitive/ behavioral/emotional \n considerations

**Self-worth strongly influenced by weight/shape**

* Criticism from family/peers regarding weight related to drive for thinness, disturbed body image
* Perfectionism and personal inadequacy lead to excessive concern about weight
* Behaviors that achieve/maintain thinness (AN)
* Negatively reinforced by reduction of anxiety about gaining weight
* Positively reinforced by comments from others
* Positively reinforced by sense of mastery/self-control over eating behavior

Behaviorally reinforcing binge-purge cycles (BN)

* After binging, disgust with oneself and fear of gaining weight lead to compensatory behavior
* Purging temporarily reduces anxiety/negative affect about weight gain
* Cycle lowers self-esteem, triggers further binging and purging

Emotion

* Low tolerance for negative affect (binge an attempt to regulate?) and/or more intense negative emotion \n experience
* **Difficulty distinguishing between positive emotions**

Etiology: Sociocultural factors

Why so many more...

* Females than males?
* White people than people of color? More Westernized regions?
* Rich people?
* Media

Chapter 10: Substance Use Disorders

Percentage of U.S. population reporting substance use in the past month (2018)

Alcohol -→ 51.1% \n Cigarettes -→ 17.2% \n Marijuana -→ 10.1% \n Psychotherapeutics (misuse) -→ 2.0% \n Cocaine -→ 0.7%

Two key symptoms

Tolerance

* Larger doses of drug needed to produce desired effect
* Effects of drug decrease if usual amount is taken

Withdrawal

* Negative physical and psychological effects from stopping substance use
* Effects specific to the substance (often physiological)

Substance use disorder DSM-5 criteria

Problematic pattern of use that impairs functioning and is associated with 2+ of the following within a 1-year period:

* Failure to meet obligations
* Repeated use when it is potentially dangerous
* Repeated relationship problems
* Continued use despite problems caused by the substance
* Tolerance
* Withdrawal
* Substance taken for a larger time or in greater amounts than intended
* Efforts to reduce or control use unsuccessfully
* Much time spent trying to obtain the substance
* Social, hobbies, or work activities given up or reduced due to use
* Craving to use the substance
* Severity ratings: Mild=2-3 criteria, Moderate=4-5, Severe 6+

Substances overview

Six MAJOR categories of substances:


1. Alcohol
2. Tobacco
3. Marijuana
4. Opiates
5. Stimulants
6. Hallucinogens

Alcohol use disorder

“Dependent” or addicted

* People who develop tolerance or withdrawal
* Alcohol withdrawal
* Muscle tremors, elevated pulse, blood pressure, and temperature
* Delirium tremens
* Rare withdrawal symptom when alcohol in blood drops suddenly
* Delirium, tremulous, hallucinations

Alcohol use disorder prevalence and co-occurrence

\
* Prevalence varies by gender, race, and education level
* Men more likely than women (8.7% men, 3.4% women over 26 years) — this is shrinking over time
* More common in divorced or never married


* Associated with other substance use – 80-85% smoke tobacco
* Commonly co-occurs with mood, anxiety, personality disorders and schizophrenia, as well as other drug use disorders
* Alcohol use particularly frequent among college students
* 39.4% report binge drinking (5+ drinks in a short period/\~1 hour)
* 12.5% report heavy drinking (5+ drinks on one occasion, 5+ times in 30 days)

Alcohol use disorder short-term effects

Absorbed into blood, metabolized by liver slowly (1 oz of 100 proof per hr)

* Depends on body composition, though
* Depends on how much drinking...
* 12 oz beer = 5 oz wine = 1.5 oz shot

Neural actions

* Stimulates GABA receptors (may reduce tension)
* Increases levels of serotonin and dopamine (may result in pleasurable effects)
* Inhibits glutamate receptors (may result in cognitive slowing)
* Effects on anterior cingulate and orbitofrontal cortex may result in problems with monitoring errors

Alcohol use disorder long-term effects

Affects nearly ever organ and tissue in long-term

* Common problems
* Impaired digestion, e.g., B-complex deficiency leads to amnestic syndrome
* Breakdown of proteins leads to cirrhosis of liver \n

Can lead to problems with:

* Endocrine
* Brain
* Pancreas
* Heart failure
* Erectile dysfunction
* Hypertension
* Stroke
* Capillary hemorrhages

\n Research hasn’t found benefit of moderate levels of drinking, despite popular belief.

Fetal alcohol syndrome (FAS)

* Heavy alcohol consumption during pregnancy
* Leading cause of intellectual disability
* Growth of fetus slows
* Cranial, facial, and limb anomalies are common
* Even moderate drinking can lead to fetal problems
* NIAAA recommends no alcohol use during pregnancy

Tobacco use disorder

* In 2018, prevalence was 17% (down from 43% in 1964)
* Still, smoking single most preventable cause of death in USA
* Those most likely to smoke are those with psychopathology
* More prevalent among under-resourced \n communities
* More men than women
* African American cigarette smokers – less likely \n to quit, more likely to get lung cancer
* AND... more likely to smoke menthol cigarettes
* Direct advertisement to this community
* People tend to inhale more deeply and hold the smoke for longer

Tobacco use disorder

Neural actions

* Nicotine stimulates dopamine neurons in mesolimbic areas
* Reinforcing properties

Long-term effects

* Emphysema
* Cancers of larynx and esophagus, pancreas, bladder, cervix, stomach
* Complications during pregnancy and sudden infant death syndrome
* Periodontitis disease
* Cardiovascular problems
* Lots of problems associated with in-taking secondhand smoke

What about e-cigarettes (vaping)?

* Look like cigarettes except
* Are made of plastic or metal
* Can be filled with liquid nicotine that is mixed with other chemicals and often with flavors


* People inhale and exhale vapors (“vaping”)
* Use has been increasing
* Doubled among high school students from 2017‒2019
* Among young people, those who vape are more likely to take up smoking cigarettes
* May also help people to quit smoking, since nicotine levels can be reduced over time and can be less toxic than combustible cigarettes
* FDA regulations treat e-cigarettes like other regulated tobacco products

Marijuana Use Disorder Overview

Most frequently used (federally-defined) illicit drug

* Legal for medicinal use in all but 8 states and legal for all uses in 11 states
* Men more likely to use than women
* Fairly equivalent across ethnic and racial groups
* Rates of daily use increasing
* May be related to varying degrees of legal status by state
* Concerning trend of increasing marijuana vaping rates among high school students

Marijuana use disorder

Major active chemical is THC (a cannabinoid)

* More potent, used in larger amounts than in past decade

Neural effects

* Cannabinoid receptors located throughout the body
* High number in hippocampus, amygdala, anterior cingulate, temporal lobe

Psychological effects

* May result in initial feelings of relaxation or sociability
* Large doses result in rapid shifts in emotion, dull attention, fragment thoughts, impaired memory, slow perceived passage of time
* Very large doses can induce hallucinations, extreme panic, cognitive impairments

Marijuana use disorder physical consequences

Short-term

* Bloodshot, itchy eyes
* Dry mouth/throat
* Increased appetite
* Reduced pressure in the eye
* Raised blood pressure

Long-term

* Impaired function/structure of lungs
* Can develop tolerance and/or withdrawal (restlessness, anxiety, tension, stomach pains, insomnia)
* Cognitive problems linked to effects on cannabinoid receptors in brain (e.g., hippocampus)
* Different patterns of amygdala-frontal cortex connectivity in users vs non-users

Marijuana use

Therapeutic effect

* Reduce nausea and loss of appetite accompanying chemotherapy
* Can relieve discomfort associated with glaucoma, chronic pain, muscle spasms, seizures, and AIDS

Legalization

* Despite some state laws, federal law prohibits dispensing marijuana for medicinal purposes
* Medical marijuana legalization not associated with increased use among teens

Opiate use disorder

Include opium and its derivatives: morphine, heroin, codeine, hydrocodone, oxycodone

* Moderate doses reduce pain
* More than ½ million people addicted to heroin, significant increase in past 5 years
* 50 years ago, primarily men in urban areas using heroin
* Heroin use now more common in less urban areas among men and women, following prescription abuse
* Prescription pain medications among the most abused of all drugs
* 7% of U.S. misused at least once
* More common among men
* More common among white and Native American populations

Opiate use disorder effects

Psychological effects

* Euphoria
* Drowsiness
* Lack of coordination
* Reduced worry
* Greater self-confidence, loss of inhibition
* Severe let-down after 4-6 hrs

Neural effects

* Stimulate receptors of the body’s opioid system
* May have a link with dopaminergic regions
* Or nucleus accumbens, but independently of dopamine

Physical Effects

* Associated with tolerance
* Associated with withdrawal—can occur within 8 hours after tolerance develops
* Muscle pain, sneezing, sweating, tearful, yawning – similar to flu
* Within 36 hours, more severe—poor sleep, nausea, vomiting, diarrhea, muscle \n twitching, chills, rise in blood pressure, heart rate
* Persist 72 hours, then diminish over 5- to 10-days
* Problems associated with use—$200 per day habit
* Resort to get money by any means necessary
* Risk of intravenous drug use related infection, such as HIV, hepatitis

Stimulant use disorder

wo classes:


1. Amphetamines (& methamphetamine) → synthetic
2. Cocaine (& crack) → derived from coca leaf

Stimulant use disorder: Amphetamines

Neural effects

* Release of norepinephrine and dopamine (while blocking their reuptake)

Short-term effects

* Wakefulness, intestinal function inhibited, appetite reduced, euphoria, energy, self-confidence
* Larger doses associated with nervousness, agitation, confusion
* Very heavy use associated with extreme suspicion and hostility

Methamphetamine

* Most commonly abused
* Men more than women
* More in small towns than urban
* Chronic use damages serotonin and dopamine systems, reduction in brain volume, damage to areas involving reward and decision-making

Stimulant use disorder: Cocaine

* 5.5 million in 2018
* Men more than women
* Neural effects
* Acts rapidly on brain
* Blocks reuptake of dopamine in mesolimbic areas

Short-term effects

* Increase sexual desire, produce feelings of self-confidence, well-being
* High quantities can lead to chills, nausea, insomnia, paranoia, hallucinations
* Poses a big risk to fetus if taken during pregnancy

Overdose

* Chills, nausea, insomnia, paranoia, hallucinations, possibly heart attack and \n death

Hallucinogen use disorder

* Includes LSD, PCP (angel dust), ecstasy’
* More men than women
* More often used by white Americans
* Act on serotonin system
* Effects take place within 30 minutes, last up to 12 hours
* Hallucinations, sense of time, mood swings, expanded consciousness
* Flashbacks—visual recurrences of perceptual experiences after effects of drug \n have worn off

Hallucinogen use disorder

\
LSD

* Popular in 1960s, regular use has declined
* No evidence of withdrawal, but tolerance develops rapidly

PCP

* Angel dust
* Declining usage
* Causes severe paranoia and violence
* Coma and death are possible

Ecstasy

* Contains both hallucinogen and amphetamine compounds – classified in own DSM-5 category (other hallucinogen use disorder)
* Pill or powder form
* Average age of first use: 21
* Increases feelings of intimacy, insight, positive emotions, self-confidence
* Can also cause muscle tension, nausea, anxiety, depression, confusion, depersonalization

Genetic factors

* Genetic factors more significant for frequent use/abuse than non-problematic use


* Family history of substance use disorder is large risk factor
* 8-fold increase risk of substance use disorder among relatives of probands with substance use disorder
* Greater concordance in MZ than DZ twins for drug use disorders in general
* Children of problem drinkers 4-5x more likely to develop alcohol use disorder
* Heritability of alcohol use disorder = 0.40-0.60
* Likely gene-environment interaction
* Genetic and shared environmental factors seem the same regardless of drug; same for men/women

Neurobiological factors

Most stimulate dopamine system, especially mesolimbic pathway (pleasure/reward)

* People may take drugs to avoid bad feelings
* Avoidance of withdrawal symptoms
* Explains frequency of relapse
* Vulnerability model vs. toxic effect model
* Vulnerability in dopamine system → substance use or substance use → dopamine system problems
* Incentive-sensitization theory
* Distinguish wanting from liking
* Dopamine system becomes sensitive to drug and associated cues (e.g., needles, rolling papers, etc.)
* Over time, liking/pleasure decreases, but wanting remains intense
* Craving (wanting) associated with use
* Cues for drug activate reward and pleasure areas of the brain involved in drug use

Neurobiological factors

Valuing short-term over the long-term

* Immediate (short-term) vs. delayed (long-term) rewards
* People dependent on substances discount delayed rewards more steeply than do people \n not dependent
* Valuing immediate vs. delayed rewards recruit different brain regions:
* Delayed reward = prefrontal cortex
* Immediate reward = amygdala, nucleus accumbens

Risky decision-making

* People with drug or alcohol use disorders are more prone to make risky decisions that can \n lead to use of substances or drug-seeking behavior
* Low tolerance for ambiguous risks (but not known risks) predicts opioid use relapse
* Neural regions supporting delay discounting and decision making have been identified

Psychological influences

Emotion regulation

* Dampen down thoughts of rejection in social situations
* Provide relief or distraction from negative emotions
* Increase positive emotions when bored \n

Expectancies about a drug’s effect predict increased drug use in general

* People who expect alcohol to reduce stress and anxiety are most likely to drink
* Expectancies about a drug’s effect predict increased drug use in general
* Expectancies about social effects may be particularly impactful among adolescents and young adults \n

Personality factors predicting onset of substance use disorders

* High levels of negative emotionality or neuroticism
* Persistent desire for arousal and positive affect
* Low constraint (high constraint = harm avoidance, conservative moral values, cautious behavior)