PSC 168: Abnormal Psychology Midterm 2

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CHAPTER 13 Disorders of Childhood

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CHAPTER 13 Disorders of Childhood

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Early life origins of psychopathology

age of onset peaks at teenage years and then another time in adulthood

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developmental psychopathology

focuses on the disorders of childhood within the context of development over the life span, enabling us to identify behaviors that are considered appropriate at one stage but not at another

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Frameworks and the structure of childhood disorders

Developmental psychopathology

  • The study of disorders of childhood within the context of life-span development

  • Enabling us to identify behaviors that are considered appropriate at one stage but not at another

  • Two broad domains: Externalizing and Internalizing disorders

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Childhood disorders are often divided into two broad domains:

  • Externalizing disorders are characterized by more outward-directed behaviors, such as aggressiveness, noncompliance.

    • aggressiveness, noncompliance, overactivity, impulsiveness

    • ADHD, Conduct Disorder

  • Internalizing disorders are characterized by more inward-focused experiences and behaviors, such as depression, and social withdrawal.

    • depression, social withdrawal, anxiety

    • Examples: Childhood anxiety and mood disorders

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The Role of Culture in Internalizing and Externalizing Behaviors

  • there are more differences between the prevalences of internalizing and externalizing problems within a culture or society than there are among societies.

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Intermittent explosive disorder (IED)

recurrent verbal or physical aggressive outbursts that are far out of proportion to the circumstances. What distinguishes IED from conduct disorder is that the aggression is impulsive and not preplanned toward other people

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Conduct Disorder DSM-5 criteria

A repetitive and persistent pattern of behavior in which the basic rights of others or societal norms or rules are violated, as manifested by the presence of at least three symptoms in the past 12 months, with at least one criterion present in the past 6 months:

  • Aggression to People & Animals

  • Destruction of Property

  • Deceitfulness or Theft

  • Serious Violation of Rules

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Conduct Disorder DSM-5 criteria

Causes impairment in social, academic, or occupational functioning.

  • If 18+ years of age, criteria are not met for antisocial personality disorder.

  • Specifiers:

    • Childhood-onset type

    • Adolescent-onset type

    • With limited prosocial emotions (i.e., 2+ of: lack of remorse/guilt, callous — lack of empathy, unconcerned

    • about performance, shallow/deficient affect)

  • Personal distress is not mentioned and it could be related to poor outcomes

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Oppositional Defiant Disorder (ODD)

ODD is diagnosed if a child does not meet the criteria for conduct disorder—most especially, extreme physical aggressiveness

  • ODD and ADHD frequently occur together, but ODD is different from ADHD in that the defiant behavior is not thought to arise from attentional deficits or impulsiveness.

  • Children with ODD are more deliberate in their unruly behavior than children with ADHD.

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Conduct Disorder - Clinical Description, Prevalence, and Prognosis

  • 5-6% prevalence in the general population, but WAY higher in juvenile justice system (59%)

  • 3-4x as many males as females

  • Also gender differences in ways displayed

    • Males more overt, girls more covert/relational

  • defined by the impact of the child’s behavior on people and surroundings.

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Defining Conduct Disorder

a pattern of repeated destructive and harmful behavior that can take different forms, including:

  • Aggressive behavior (e.g., bullying, physically hurting animals or people)

  • Destroying property (e.g., vandalizing a building, setting a fire)

  • Lying or stealing (e.g., shoplifting, breaking into a house and stealing items, lying about behavior)

  • Breaking rules (e.g., skipping school, missing curfew)

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Conduct Disorder (CD) Comorbidities and Longitudinal Course

The researchers found that conduct disorder symptoms at age 3 predicted conduct disorder symptoms at age 6, even when symptoms of ADHD and ODD were controlled for.

  • Anxiety and depression are common

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Conduct Disorder (CD) prevalence and Prognosis

  • prevalence rates between 5% and 6%.

  • CD is more common in boys than in girls

  • prognosis for children diagnosed with conduct disorder is mixed.

    • men and women with the life-course-persistent CD will likely continue to have all sorts of problems in adulthood, including violent and antisocial behavior.

    • CD in childhood does not inevitably lead to antisocial behavior in adulthood

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Genetic Influences of Conduct Disorder

  • evidence for genetic influences are mixed- heritability likely plays a part.

  • aggressive behavior (e.g., cruelty to animals, fighting, destroying property) is more heritable than other rule-breaking behavior

  • combination of conduct problems and callous and unemotional traits is more highly heritable than conduct problems alone

  • parenting of the adoptive mother (gave a lot of positive reinforcement) appeared to act as a buffer against the genetic propensity

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Neurobiological Influences of Conduct Disorder

  • Parenting can also contribute to the exacerbation of callous and unemotional traits

  • particularly those with callous and unemotional traits, seem to be deficient in this moral awareness, lacking remorse for their wrongdoing

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Treatment of Conduct Disorder

Family Interventions

  • family checkup (FCU) has been shown to have positive effects in preventing conduct problems and aggression in children.

  • involves 3 meetings to get to know, assess, and provide feedback to parents regarding their children and parenting practices

  • parent management training (PMT): parents are taught to modify their responses to their children so that prosocial behavior is consistently rewarded.

Multisystemic Treatment

  • involves delivering intensive and comprehensive therapy services in the community, targeting the adolescent, the family, the school, and, in some cases, the peer group

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Oppositional Defiant Disorder (ODD) facts and stats

ODD

  • 8.3% lifetime prevalence (slightly higher for males, lower for females in some studies)

  • If left untreated, 52% continue to have it 3 years later

  • And about ½ of that 52% will go on to have CD

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ODD & CD comorbidity

  • All are highly comorbid with one another, as described nearly 25% of children with ODD go on to have CD

  • About 1/3 of children with ADHD have ODD, and about ½ of those go on to have CD

  • Substance abuse more likely in children with CD

  • Learning disorders more likely in children with ODD, ADHD, CD

  • Depression, anxiety common in those with CD (15-45%)

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Moffitt and colleagues have provided a good deal of evidence for two types of conduct disorder. The____ type is associated with an early age of onset and continued problems into adolescence and adulthood. The____ type begins in the teenage years and is hypothesized to remit by adulthood, though a recent follow-up study has not supported the idea that this type remits.

life-course persistent, adolescent-onset;

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Comorbidity is common in conduct disorder. Other problems that co-occur with conduct disorder include_____,,, and____.

ADHD, substance abuse, depression, anxiety

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Antisocial personality disorder (ASPD)

Personality disorder (we’ll talk more in a few weeks)

  • Diagnosed after age 18

  • Characterized by aggressive antisocial behaviors beginning by age 15 and continuing into adulthood

  • Failure to conform to norms with regard to lawful behavior

  • Deceitfulness (lying, conning, using aliases)

  • Impulsivity or failure to plan ahead

  • Reckless disregard for safety of self or others

  • Consistent irresponsibility

  • Lack of remorse

Psychopathy — not a DSM diagnosis

  • Interpersonal trait

  • Deceitful, callous, unremorseful, impulsive, unemotional, glib

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Trajectories of ODD, CD, ASPD? Sometimes...

•Unspecified Disruptive Behavior Disorder → ODD → ADHD → CD → ASPD \n - Heterotypic continuity - one disorder increases likelihood of a different disorder

  • But not always! Only ~40% with Conduct Disorder → Antisocial Personality Disorder

  • Which kids go on to have the MOST problems? Which kids don’t “get better”?

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Predictors of negative trajectory from one externalizing disorder to another

  • Early onset

  • Family history of ODD, CD, ASPD

  • Parent substance abuse, mood disorders

  • Permissive and/or harsh parenting—or worse, a mix of the two!

  • Low SES

  • Violent neighborhood

  • Comorbid LD or ADHD

  • Marital conflict

  • Child maltreatment

  • Presence of Callous/Unemotional Traits - less sensitive to punishment and reward

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Etiology: OD Disorder

Early onset associated with

  • Parent substance abuse

  • Parent incarceration

  • Parent mood disorders

  • Parent ASPD

Perhaps heritability is for traits

  • Irritability

  • impulsivity

  • Sensation seeking

    these traits may be inheritated less so the diagnosis

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Etiology: Conduct Disorder

Genetics: Heritability of about 53%

Cognitive Factors

  • Deficits in verbal reasoning, executive function

  • Difficulty perceiving distress

  • Deficits in social information processing (hostile bias)

Neurobiological Differences

  • Reduced activation in amygdala, vmPFC, insula, ventral striatum, orbitofrontal cortex

  • Less responsiveness to reward — esp. with CU traits

  • Reduced serotonin and cortisol, lower HR (lower arousal?)

Family/Contextual Influences

  • Family conflict

  • Lower SES

  • Low parental monitoring and unpredictable discipline

  • Peer Influences

  • Peer rejection

  • Association with deviant peers — modeling? Coercion? GxE? on? GxE?

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Earlier vs. later onset CD

Early onset (“life-course persistent”)

  • Present before age 10 years

  • More persistent, more pervasive

  • More ADHD symptoms, neuropsychological deficits, more academic problems, more family dysfunction, more aggression/violence

  • More than 90% had/have ODD

Later onset (“adolescent-limited”/“adolescent onset”)

  • Present after age 10 years

  • Less impairment than early onset

  • More rule-violating than aggressive behaviors

  • Often remit before adulthood (“adolescent limited” — Moffitt); less severe outcomes, “maturity gap”?

  • Probably caused by peer influences

  • More common—an exaggeration of normal development?

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Treatment of Conduct Disorder

Medications?

  • NOPE!

  • Mood stabilizers, antipsychotics often prescribed for HIGHLY aggressive children, but all “off label”

Psychosocial

  • Big focus is on reinforcements of behavior

  • Try to set up ways to reduce reinforcement of undesired behavior

  • Examples of unintended positive reinforcement:

    • Aaron is currently in room with brother, room is empty except for toy.

    • Aaron is BORED, wants attention, but brother is busy with toy.

    • Aaron hits brother.

    • Mother runs to room to see why brother is crying.

    • Mother yells at Aaron and talks to him about why hitting is wrong.

    • Aaron is LOVING IT because this is not BORING, and he gets attention.

    • Better solution? -→ TIME OUT

  • 3 biggest, most efficacious:

    • Parent-management training (PMT)•Multisystemic Treatment (MST)

    • Collaborative Problem Solving

    • Each focus on broader contexts of bad behavior

    • PMT focus on family

    • MST focus on all context—family, school, neighborhood, culture•Preventative?•Head Start

    • Community-based prevention program for low-income families•Ongoing challenge: How to sustain gains beyond preschool

  • Fast Track - INTENSIVE

  • Family Checkup for high-risk toddlers

  • 3 brief meetings → less disruptive behavior even 2 years later

years later

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ADHD - Attention-deficit/hyperactivity disorder

  • Developmentally inappropriate levels of (a) inattention and/or (b) hyperactivity-impulsivity, interferes with functioning

  • Median age at diagnosis = 7 years

  • Prevalence: 5-8% -- less prevalent in females than males

  • Heritability: 0.7-0.8

  • Often persists into adulthood; long-term impairments common

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DSM-5 symptoms of ADHD

Inattention

  • Careless mistakes

  • Difficulty sustaining attention

  • Doesn’t listen

  • Difficulty with follow through, completing tasks

  • Organizational challenges

  • Dislikes/avoids activities requiring sustained mental effort

  • Loses things

  • Easily distracted

  • Forgetful

Hyperactivity-Impulsivity

  • Fidgeting/squirming

  • Difficulty remaining seated

  • Running/climbing excessively

  • Difficulty playing/engaging in leisure activities quietly

  • “On the go”, “driven by a motor”

  • Talks excessively

  • Blurting out answers

  • Difficulty waiting turns

  • Interrupts/intrudes

*has to have 6 from either subtype or 12, 6 form each.

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How to diagnose ADHD

  • Symptoms prior to age 12 - inattention presentation is usually diagnosed later and girls have this tendency more

  • Symptoms present across settings

  • Interfere with social, school, work functioning

  • Symptoms can’t be better explained by another mental disorder

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ADHD presentations

  • Used to be called subtypes

  • Inattentive presentation: 6+ inattentive symptoms, fewer than 6 hyperactive-impulsive symptoms

  • Hyperactive-impulsive presentation: 6+ hyperactive-impulsive symptoms, fewer than 6 inattentive symptoms

  • Most often limited to the preschool period then → Combined

  • Combined: 6+ inattentive AND 6+ hyperactive-impulsive symptoms

  • For adults (ages 17yo+): Only 5 symptoms in a given category required

-→ lowered threshold because a lot of the symptoms apply to children as they lose it developmentally

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Comorbidities of ADHD – VERY COMMON

  • Oppositional defiant disorder (ODD) -→ 30-50%

  • Conduct disorder -→ 3.5-10%

  • Anxiety and depression-→ ~30% have a comorbid internalizing disorder

  • Learning disorders -→ 10-70%

  • Substance use disorders

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Girls with ADHD

  • Childhood prevalence of ADHD in boys is 2-2.5 times higher than in girls; by adulthood, ratio is closer to equal

  • Females more likely to present inattention symptoms and internalizing problems, males more likely to display hyperactive-impulsive symptoms and externalizing problems

In childhood...

  • Viewed more negatively by peers

  • Exhibited a range of neuropsychological deficits, particularly in executive functioning (e.g., planning, solving problems)

By adolescence...

  • More likely to have symptoms of an eating disorder and substance abuse

  • Self-harm emerges as a key concern

By early adulthood...

  • Young women who continued to meet diagnostic criteria for ADHD were more likely to have internalizing and externalizing psychopathology

  • More likely to have unplanned pregnancies, lower academic achievement, and greater substance use due to risky decisions

  • ADHD highly impairing in girls during childhood and adolescence, with persisting difficulties through adulthood

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Etiology: Genetic influences of ADHD

Adoption and twin studies

  • Heritability estimates as high as 70 to 80%

  • Several candidate genes implicated-→ DRD4, DRD5, DAT1

    • Dopamine genes

      • Associated with increased risk only when prenatal maternal nicotine or alcohol use is \n present

    • SNAP-25

      • Codes for protein that promotes plasticity

  • BUT... GWAS studies have not always found \n the same genes and many genes identified \n are not specific to ADHD

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Etiology: Neurobiological influences of ADHD

Individuals with ADHD show differences in brain structure, function and connectivity

  • Dopaminergic areas smaller in children with ADHD

    • E.g. amygdala, hippocampus, caudate nucleus, nucleus accumbens, putamem

Poor performance on tests of frontal lobe function (executive functioning/cognitive control)

  • Inhibiting automatic responses

  • Working memory

  • Planning ahead

  • Organizational skills

Differences in reward processing

  • Preference for smaller, sooner over larger, later rewards

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Etiology: Prenatal/birth factors ADHD

Low birth weight - 3x as common in children with ADHD

  • Can be mitigated by later maternal warmth!

  • Brain damage during pregnancy/delivery increases ADHD incidence

  • higher blood levels of lead may be associated to a small degree with symptoms

  • White matter abnormalities due to birth injuries

  • BUT most children with ADHD don’t have this history

  • Maternal smoking during pregnancy linked with ADHD symptoms

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Etiology: Environmental factors ADHD

Environmental toxins

  • Limited evidence that additives may influence ADHD symptoms

  • No evidence that refined sugar causes ADHD

  • Maternal smoking

  • Lead exposure in early environment

  • Difficult to study

  • Prenatal and postnatal complications

  • Severe neglect/institutional deprivation -→ Romanian orphanage studies

  • GxE interactions

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Family Factors in ADHD

  • parenting practices may contribute to maintenance or exacerbation of symptoms and to consequences of ADHD

  • however, there is little evidence to suggest that families cause ADHD

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Treatment Of ADHD

Combination (medication+behavior) and carefully monitored and titrated medication alone superior to behavioral alone and community \n care for core symptoms

  • Benefit of medications did not persist beyond the study

  • Combination superior for improvements in other domains (anxiety, academic performance, social skills, parent-child relationship)

  • Academic interventions also relevant

Medication interventions

Stimulants (Ritalin, Adderall, Concerta, Strattera)

  • Reduce disruptive behavior, aggression, and impulsivity

  • Improve ability to focus attention

  • Improve concentration, goal-directed activity, classroom behavior

Non-stimulant

  • Used when stimulants are not appropriate (e.g., cardiac conditions, tics)

  • Atomaxatine (inhibits reuptake of NE)

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Depression in children - Clinical Descriptions

Children ages 7-17 and adults symptoms:

  • depressed mood, inability to experience pleasure, fatigue, concentration problems, and suicidal ideation.

  • Children and adolescents differ from adults in showing more guilt but lower rates of early-morning wakefulness, early-morning depression, loss of appetite, and weight loss.

  • these guidelines also recommend that impairment be identified in two different settings (e.g., home and school)

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Prevalence of Depression in children

The prevalence among adolescent girls (15.9%) is almost twice that among adolescent boys (7.7%)

  • There is evidence that comorbidity between depression and anxiety in adolescence may be caused in part by shared genetic vulnerabilities

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Etiology of Depression in Childhood and Adolescence

  • individuals who had a short allele of the serotonin transporter gene and had experienced significant stressful interpersonal life events were more likely to have a major depressive disorder episode

  • early adversity (e.g., financial hardship, maternal depression, chronic illness as a child) predicted depression from age 15 through age 20

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Treatment of Childhood and Adolescent Depression

  • cognitive behavior therapy (CBT) and interpersonal therapy are effective treatments for depression in adolescents

  • treatment consisting of both CBT and Prozac was the most effective

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History of Autism

ASD first described by Leo Kanner in 1943: \n “early infantile autism”

  • Not in DSM until 1980 (DSM-III)

  • Prior to this, ‘schizophrenia’ or ‘psychosis’

  • Autistic Disorder and Asperger’s Disorder in \n ‘Pervasive Developmental Disorder’ category \n until DSM-5

  • Now subsumed under ‘Autism Spectrum Disorder’

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Autism Spectrum Disorder: Prevalence

  • prevalence rate of ASD in the United States 1 in 54 children

  • diagnostic criteria have broadened between DSM-III and DSM-5

  • Average age of diagnosis: 4.4 years

  • Reliable diagnoses can be made as early as 18-24 months in some cases

  • Affects all socioeconomic, ethnic, racial groups (but there are inequities)

  • Occurs 4x more often in boys than girls

  • Comorbidities common: Intellectual disability, epilepsy, sleep problems, ADHD, anxiety

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True increase in Autism Diagnosis

Autism not formally recognized in DSM until 1980

  • Broadening of diagnostic criteria in DSM-IV (1994), and even more in DSM-5 \n (2013)

  • Children diagnosed younger

  • Increased public awareness (“autism epidemic”)

  • Incentive for diagnosis, “diagnostic substitution”

  • But... studies have found increased rates can’t be explained by diagnostic practices alone – environmental influences?

  • And... most recent prevalence estimates showed marked increase in rates among racial and ethnic minority groups – addressing inequities?

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Social development for Autism

  • Infancy: Early emerging and highly conserved predisposition to social engagement and adaptation

  • In ASD: Predisposition to orient to and engage with people are absent, impaired, or diminished. Preference for objects.

  • Over time, developing into “experts in people” versus “experts in things”

  • How might this impact development over a lifespan?

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How is ASD diagnosed?

No definitive medical test

  • Interviews, observation, behavior checklists, standardized cognitive and psychological tests

  • Medical work-up important; best practice involves genetic testing

  • Rule out hearing impairment, other behavioral disorders (e.g., ADHD, anxiety), etc.

  • Developmental and intellectual assessment

  • Rate of intellectual disability in ASD estimated at 25-30%

  • Nonverbal often > than verbal

  • Patterns over time variable

  • Approximately 50% of children with ASD demonstrated relative improvements

  • Around 25% demonstrated declines

  • Adaptive assessment

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Inequities in diagnosis in Autism

Historically...

  • White children ~19% more likely than Black children, 65% more likely than Hispanic children to be diagnosed (Durkin et al., 2017)

  • But... Black and white parents report first concerns when children are about the same \n age (Jang et al., 2014) \n •SES doesn’t fully explain differences in prevalence across race/ethnicity \n •Disparities? Inequities? \n •More recent trends from CDC... \n •Prevalence similar across racial and ethnic groups \n •Higher proportion of Black children classified as having intellectual disability n compared with White and Hispanic children

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Anxiety vs fear

Anxiety/Worry (example: GAD)

  • Anxiety is defined as apprehension over an anticipated problem.

  • Future-oriented mood state

  • Characterized by marked negative affect

  • Somatic symptoms of tension NOT fight or flight

  • Apprehension about future danger or misfortune \n

Fear (example: phobia)

  • Present-oriented mood state, marked negative affect

  • Immediate fight or flight response to danger or threat

  • Strong avoidance/escapist tendencies

  • Abrupt activation of the sympathetic nervous system

  • In contrast, fear is defined as a reaction to immediate danger. Fear tends to be about a threat that is happening now, whereas anxiety tends to be about a future threat

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‘Normal’ to ‘disordered Anxiety

Characteristics of Anxiety Disorders

  • What takes normal worry or anxiety to the level of a disorder

  • psychological disorders – Pervasive and persistent symptoms of anxiety and fear

  • Involve excessive avoidance and escapist tendencies

  • Causes clinically significant distress and impairment

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Pathological anxiety

Anxiety is evolutionarily related to fear and is often discussed as if it is the same biologically

  • Same, but different...

  • In anxiety, more cognitive factors involved

  • Disorder associated with overestimation of threat and underestimation of coping resources

  • Often involves attempts to control mood, thoughts, or environment.

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What’s common to all core anxiety disorders?

For each disorder, the following DSM-5 criteria must be met (with added criteria specific to each disorder)

  • Symptoms interfere with important areas of functioning or cause marked distress

  • Symptoms not caused by a drug or medical condition or psychiatric condition

  • Symptoms persist for 6 months (only 1 month for panic disorder)

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Comorbidity of Anxiety

  • More than 50% of those with anxiety disorder meet criteria for another anxiety disorder

  • 75% of those with anxiety disorder meet criteria for another psychological disorder — 60% also have depression; obsessive compulsive disorder also \n common

  • Comorbidity is associated with greater severity and poorer outcomes of the \n anxiety disorders

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Common treatment elements of Anxiety

Exposure

  • Face the situation or object that triggers anxiety

  • E.g., exposure hierarchy: graded exposure to a list of triggers

  • Effective for 70–90% of clients

  • Behavioral view: Newly learned associations inhibit fear

  • Cognitive view: Corrects mistaken beliefs

  • Virtual reality vs. in vivo (real-life) exposure are equally effective

  • Mindfulness and acceptance treatments also show promise

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A note about medications for Anxiety

Anxiolytics: drugs that reduce anxiety

  • Benzodiazepines (e.g., Valium, Xanax) – sedatives/minor tranquilizers

    • Can be addictive and cause severe withdrawal symptoms

    • Side effects: cognitive and motor difficulties → accidents, etc

  • Antidepressants (e.g., SSRIs, SNRIs)

    • More effective than placebo

    • Side effects: jitteriness, weight gain, elevated heart rate

      • Lots stop taking them because of these

  • Only help as long as they’re taken; most people relapse once they stop taking medications

  • Psychological treatments are considered the preferred treatment of most anxiety disorders

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Generalized anxiety disorder (GAD)

DSM-5 Criteria

  • Excessive anxiety and worry at least 50% of the day about a number of events/activities \n (e.g., family, health, work, school, finances, etc.

  • The individual finds the anxiety/worry difficult to control

  • The anxiety/worry are associated with at least 3 of the following (only one needed for children):

    • Restlessness or feeling “keyed up” or on edge

    • Easily fatigued

    • Difficulty concentrating or mind going “blank”

    • Irritability

    • Muscle tension

    • Sleep disturbance

  • Must occur more days that not for 6 months or more

  • Causes clinically significant distress or impairment

  • Not attributable to use of a substance or medical condition or psychiatric condition

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GAD facts and stats

  • Affects 3-4% of the general population

  • Females outnumber males approximately 2:1

  • Exists across cultures, but may manifest differently

  • Onset often in adolescence (though many report worrying all their lives)

  • Often chronic, running a life-long course

  • Tendency to be anxious runs in families – heritability around .33

  • Commonly comorbid with other anxiety disorders and depression

  • More associated with ANXIETY than fear

  • When you think about GAD, think “worry” and “rumination”

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GAD associated features and treatment

Associated Features

  • Avoidance of shifts in emotions (contrast avoidance model)

    • To avoid shifts, prefer constant state of worry – ”hope for the best, prepare for the worst” → more stable emotional state (even though uncomfortable)

      • Research suggests that internal verbal dialogue of worry (i.e., rumination) may act as a \n means to suppress arousal

Treatment of GAD

  • Medications

    • Benzodiazapines (e.g., Xanax, Valium)

    • SSRIs (e.g., Prozac, Paxil) often prescribed

  • Psychological intervention

    • Cognitive-behavioral therapy (CBT)

    • Relaxation training to promote calmness

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Specific Phobias

a consistent tendency to experience extreme fear of an object or situation, such as flying, snakes, or heights. The person recognizes that the fear is excessive but still goes to great lengths to avoid the feared object or situation.

  • specific phobias are highly comorbid

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Specific Phobia

DSM-5 Criteria

  • Marked, out of proportion, fear within an environmental or situational context to the presence or anticipation of a specific object or situation

  • Exposure to phobic stimulus provokes immediate anxiety (actually, fear) response, which may take the form of a panic attack (more on that soon)

  • Person recognizes fear is out of proportion

  • Phobic situation is avoided or endured with intense anxiety/distress

  • Must occur for 6 months or more (new in DSM-5)

  • Causes clinically significant distress or impairment

  • Not attributable to use of a substance or medical condition or psychiatric condition

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Specific phobia facts and stats

  • Affects 8-9% of the general population

  • Females are again over-represented

  • Exists across cultures

  • Onset typically begins in adolescence

  • Runs a chronic course (phobias don’t tend to go away without treatment)

  • Often have comorbid specific phobias—likely to fear multiple stimuli

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Common phobias

Blood-injury-injection phobia

Situational phobia

  • Public transportation or claustrophobia/fear of enclosed places (e.g., planes)

Natural environment phobia

  • Events occurring in nature (e.g., heights, storms)

Animal phobia

  • Animals and insects, snakes, spiders and dog phobias common

Other phobias

  • Do not fit into the other categories (e.g., fear of choking, vomiting)

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Treatment of specific phobia

Almost exclusively psychological in nature — highly effective

  • Exposure therapy

  • In-vivo (real life) exposure

  • Imaginal exposure

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Social anxiety disorder

DSM-5 Criteria

  • Fear or anxiety specific to social settings, in which the individual feels noticed, observed, or scrutinized

  • Typically individual will fear that they will display their anxiety and experience social rejection

  • Social interaction consistently results in distress

  • Social interaction is avoided or endured with intense anxiety/distress

  • The fear and anxiety are grossly disproportionate to the situation

  • Must occur for 6 months or more

  • Causes clinically significant distress or impairment

  • Not attributable to use of a substance or medical condition or psychiatric condition

KEY COMPONENT: Fear of evaluation

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Social anxiety disorder facts and stats

  • Affects 7% of the general population

  • Represented equally across genders

  • Exists across cultures

  • Onset typically begins in early adolescence

  • Runs a chronic course (doesn’t tend to go away without treatment)

  • Often have comorbid anxiety disorders and depression

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Social anxiety disorder is NOT just shyness

  • High impairment/disability for social phobia

  • Significant interference in work, educational attainment, and social functioning, also associated with substance abuse

  • BUT... Kagan has found a link between ‘behavioral inhibition’ (shyness) in children and later development of social anxiety disorder

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Social anxiety disorder treatment

Medication treatment

  • Beta blockers – are ineffective

  • Tricyclic antidepressants – reduce social anxiety

  • Monoamine oxidase inhibitors – reduce social anxiety

  • SSRI (e.g., Paxil) – FDA approved for social anxiety disorder

  • Relapse rates – high following medication discontinuation

Psychological treatment

  • Cognitive-behavioral treatment – highly effective•Key elements: exposure, rehearsal, role-play in a group setting

  • Preferred method of treatment now by AMA

  • Social skills training

Key elements: Extensive modeling of behaviors, reduces use of safety behaviors (e.g., poor eye contact)

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Panic disorder DSM-5 criteria

What is a panic attack?

  • A sudden onset of intense apprehension, terror, and/or feelings of impending doom

Recurrent, unexpected panic attacks (as defined before)

  • At least one attack has been followed by ONE month or more of:

  • Persistent concern or worry about the possibility of having more attacks or the consequences of attacks or behavior changes because of attacks (losing control, having heart attack, “going crazy,” etc.)

  • Significant maladaptive change in behavior related to attacks (e.g., behaviors designed to avoid having panic attacks such as avoidance of exercise or unfamiliar situations)

  • Not attributable to use of a substance or medical condition or psychiatric condition

Must be accompanied by at least 4 added symptoms:

Physical symptoms:

  • Shortness of breath

  • Heart palpitations

  • Nausea

  • Upset stomach

  • Chest pain

  • Feelings of chocking/smothering

  • Dizziness, lightheadedness, faintness

  • Sweating

  • Chills

  • Heat sensations

  • Numbness or tingling

  • Trembling

Psychological symptoms:

  • Depersonalization—feel like outside body

  • Derealization—feel like world isn’t real

  • Fear of losing control/going “crazy”

  • Fear of dying

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Panic disorder

Types of panic attacks

  • Unexpected (uncued) panic

  • Situationally bound (cued) panic

  • Situationally predisposed panic

  • NOTE: Can have a single panic attack (~25% of people will) — not the same as panic disorder

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Panic disorder facts and stats

Affects about 2.7% of the population

  • Over two times as many females as males have panic disorder

  • Exists across cultures

  • Onset often in mid- to late-20s

  • Runs an intermittent course (goes away, but comes back)

  • Often have comorbid anxiety disorders and depression

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Positive feedback loop

Can be seen as analogous to broken car alarm...

Physical Anxiety Symptoms

  • Pounding Heart

  • Increased Breathin

  • Thoughts/Cognition

  • “I’m going to die

  • “I can’t escape”

  • “I’m having a heart attack”

catastrophizing

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Agoraphobia DSM-5 criteria

Panic Disorder can occur with or without Agoraphobia

  • Agoraphobia can also occur alone (new to DSM-5), but more likely with \n panic disorder \n

DSM-5 criteria for agoraphobia

  • Disproportionate and marked fear or anxiety about at least TWO situations where it would be difficult to escape or receive help in the event of incapacitation, \n embarrassment, or panic-like symptoms

  • These situations consistently evoke fear or anxiety

  • These situations are avoided or require the presence of a companion or are endured with intense fear/anxiety

  • Symptoms must be present for 6 months or more

  • Causes clinically significant distress or impairment

  • Not attributable to use of a substance or medical condition or psychiatric condition

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Agoraphobia facts and stats

Commonly avoided situations due to agoraphobia

  • Being outside of the home alone

  • Being inside the home alone

  • Public transportation

  • Open spaces: outdoor markets, parks

  • Indoor spaces: malls, theaters, shops, cinemas, \n lecture halls

  • Standing in a crowd

  • Being in line

Facts and Stats

  • Affects 0.8% of the general population

  • About 4 times more common in females

  • Average age of onset is early adulthood

  • Rest is similar to panic disorder – intermittent, similar comorbidities

  • About 50% of people with agoraphobia experience panic attacks

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Panic disorder treatment

Medication treatment of Panic Disorder

  • Target serotonergic, noradrenergic, and benzodiazepine GABA systems

  • SSRIs (e.g., Prozac and Paxil) – Preferred drugs

  • BUT... relapse rates are high following medication discontinuation

Psychological and combined treatments of Panic Disorder

  • Cognitive-behavior therapies are highly effective

  • No long-term advantage for combined treatments

  • Best long-term outcome? Cognitive-behavior therapy!

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Anxiety in children and adolescents

  • Prevalence: 3-5% of children and adolescents

  • Similar to adults

  • Functioning must be impaired

  • Different from adults

  • Fears don’t need to be regarded/recognized as unreasonable

Why?

  • Can interfere with acquisition of developmentally-appropriate skills

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Separation anxiety disorder

  • Constant worry that some harm will befall their \n parents or themselves when they’re away from \n their parents

  • At home, children shadow one or both parents

  • Often first observed when children begin school

  • Symptoms: Distress when separated from caregiver, school refusal, fear of sleeping away from home, etc.

  • Associated with the development of other internalizing and externalizing disorders at later ages

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Etiology of anxiety disorders in \n children/adolescents

Genetic influences

  • Genes do their work via environment

    • e.g., play a role in separation anxiety in context of more negative life events

  • Parental control and overprotectiveness play only a small role

    • Only 4% of variance in childhood anxiety accounted for by parental control - statistical vs clinical significance?

  • Emotion regulation problems

  • Experiencing bullying

  • Social anxiety

    • Overestimation of danger in social situations, underestimation of ability to cope → anxiety → avoidance of social situations → fewer opportunities to develop social skills

    • Behavioral inhibition

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General treatments for anxiety in \n children/adolescents

The earlier the treatment, the more likely treatment effects are to last

  • CBT-based strategies, e.g., Kendall’s Coping Cat program

    • Confrontation of fears

    • Development of new ways to think about fears

    • Exposure to feared situations

    • Relapse prevention

    • Parents are also included in a couple of sessions

    • Used for social anxiety, GAD, separation anxiety disorder

    • When combined with medication (Zoloft), more effective than medication or Coping Cat alone for separation anxiety

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Common etiological factors across anxiety disorders- Fear is adaptive

Mammalian evolution required a perceptual system to \n identify threats and a reflexively wired motor system to \n move the organism away from danger

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Common etiological factors across anxiety disorders - Fear conditioning

Dangerous stimulus — motive emotional state (fear) and \n behavioral response (freeze, escape, attack)

  • Fear motivates response

  • Fear can be conditioned to cues associated with danger

We are more likely to fear events and situations that provided threats to the survival of our ancestors (prepared learning)

  • Deadly predators, heights, and wide open spaces

Less likely to fear frequently encountered potentially deadly objects in our contemporary environment

However, can be conditioned to fear almost anything

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Conditioning example: Mowrer’s two-factor model (1947) for Specific Phobia

  • Step 1: Classical conditioning (dog bite classically conditions fear)

  • Step 2: Operant conditioning (fear motivates person to avoid dogs)

  • Maybe phobias are a conditioned response to threat (classical conditioning)

  • ... and are sustained by avoidant behaviors (operant conditioning)

  • BUT... many people with anxiety disorders don’t report specific triggers, and many who experience threats don’t develop anxiety

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Expansions on Mowrer’s two-factor model for Anxiety

Classical conditioning could occur in other ways besides direct experience

  • Modeling – e.g., seeing a dog bite someone else, watching a video of a vicious dog attack

  • Verbal instruction – e.g., as a child, hearing your mom warn that dogs are dangerous

Some people are more prone to developing anxiety disorders than others

  • Acquire fears more readily through classical conditioning

  • Experience more persistent fears once conditioned (i.e., harder to extinguish fears)

  • Are more sensitive to unpredictable/diffuse/remote threats (vs. acute/immediate/well-defined threats)

    • People with anxiety disorders show high physiological arousal to unpredictable threat conditions (versus neutral and predictable conditions) compared to those without anxiety disorders

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Conditioning example: Interoceptive conditioning for Panic Disorder

Classical conditioning of panic in response to internal bodily sensations

  • A person experiences somatic signs of \n anxiety

  • Followed by a panic attack

  • Panic attacks become a conditioned response to somatic changes, such as those indicating poor oxygen flow

  • Slower to extinguish than nonbodily \n stimuli

Accompanied by catastrophic misinterpretation of bodily cues (cognitive)

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Example of Catastrophic Misinterpretation of Bodily Cues for Anxiety

Studies of experimentally induced panic attacks

  • Those who have panic attack on induction differ from those who don’t in one key way:

  • Degree to which they are scared ofbodily changes they are experiencing –i.e., tendency to have catastrophic \n interpretations of bodily cues

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Genes and heritability for Anxiety

  • Heritability studies suggest anxiety is 50-60% heritable

  • Genetic contribution may may be greater for females

  • Some genes may elevate risk for several anxiety disorders

    • E.g., a family member with a phobia is associated with increased risk of developing a phobia and other anxiety disorders

  • Genetic vulnerability for anxiety and depression may overlap

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Neurobiological correlates for Anxiety

Fear system

  • Activation is automatic

  • Relatively immune to cognitive influences

    • Fear affects cognitions more than it is controlled by them

    • Often know “shouldn’t” be afraid

  • Organized around the amygdala

    • Limbic structure in the medial anterior temporal lobe

    • Mediates input from cortical and thalamic sites to hypothalamic and brain stem nuclei that control various aspects of overt fear behavior

    • Anxiety disorders related to heightened activity in the amygdala, diminished activity of the medial prefrontal cortex in response to threatening stimuli

      • Connection between these areas may be atypical

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Neurobiological correlates for Anxiety

Activity of neurotransmitters

  • Disruptions in serotonin and GABA: Affects modulation of relevant brain regions (e.g., amygdala)

  • Norepinephrine: Increased levels and changes in sensitivity of receptors

HPA axis

  • Cortisol awakening response (CAR) size in adolescents predicted onset of anxiety over subsequent 6 years

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Personality/cognitive factors for Anxiety

Behavioral inhibition

  • Withdrawal, avoidance, fear of the unfamiliar, and over-arousal to novelty; beginning in childhood (as early as 4 mos of age); relatively stable trait

  • High neuroticism levels

  • Intolerance of uncertainty

  • Attention to threat

    • Tendency to notice negative environmental cues; selective attention to signs of threat

  • Belief that one lacks control over environment

  • Sustained negative beliefs about future

    • Bad things are likely to happen → Engage in safety behaviors, which maintain negative cognitions

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Integrated model for Anxiety

Integrative view

  • Genetic/biological vulnerability interacts with psychological, experiential, and social variables to produce an anxiety disorder

The problem of comorbidity

  • Comorbidity is common across the anxiety disorders

    • About half of patients have > 2 or more secondary diagnoses

    • Major depression is the most common secondary diagnosis

  • Comorbidity suggests common factors across anxiety disorders

  • Anxiety and depression are closely related (really closely related... some people think that GAD and MDD are the same thing)

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Social Anxiety Disorder

core feature of social anxiety disorder is a persistent, unrealistically intense fear of social situations that might involve being scrutinized by, or even just exposed to, unfamiliar people

  • Among people with social anxiety disorder, at least a third also meet the criteria for a diagnosis of avoidant personality disorder

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Panic Disorder

characterized by recurrent panic attacks that are unrelated to specific situations and by worry about having more panic attacks.

  • A panic attack is a sudden experience of intense apprehension, terror, or feelings of impending doom, accompanied by at least four other symptoms.

  • Physical symptoms can include shortness of breath, heart palpitations, nausea, upset stomach, chest pain, feelings of choking and smothering, dizziness, lightheadedness, faintness, sweating, chills, heat sensations, numbness or tingling sensations, and trembling

  • depersonalization (a feeling of being outside one’s body)

  • derealization (a feeling of the world not being real

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Agoraphobia

defined by anxiety about situations from which it would be embarrassing or difficult to escape if anxiety symptoms occurred. Commonly feared situations include crowds and crowded places

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Generalized Anxiety Disorder

The central feature of generalized anxiety disorder (GAD) is worry

  • The term worry refers to the cognitive tendency to chew on a problem and to be unable to let go of it

  • the worries of people with GAD are excessive, uncontrollable, and long-lasting.

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Gender Influences on the Anxiety Disorders

  • Women are more vulnerable to anxiety disorders than are men, with several studies documenting a 2 to 1 gender ratio

  • First, women may be more likely to report their symptoms

  • women show higher neuroticism levels and more biological reactivity to stress than do men

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Culture Influences on the Anxiety Disorders

cultures differ with regard to variables such as stress levels, the nature of family relationships, the presence of war, and the prevalence of poverty—all of which are known to play a role in the occurrence of anxiety disorders.

  • Countries with high levels of income inequality, such as European countries and the United States, have much higher rates of anxiety disorders than do most other regions of the world

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Fear Conditioning in anxiety disorders

Mowrer’s model suggests two steps in the development of an anxiety disorder:

  1. Through classical conditioning, a person learns to fear a neutral stimulus (the conditioned stimulus, or CS) that is paired with an intrinsically aversive stimulus (the unconditioned stimulus, or UCS).

  2. A person gains relief by avoiding the CS. Through operant conditioning, this avoidant response is maintained because it is reinforcing (it reduces fear)

does not actually fit the evidence very well, for two reasons:

  • First, many people who have anxiety disorders cannot remember any threatening event that triggered their symptoms.

  • Second, many people who do experience serious threats do not develop anxiety disorders

People with anxiety disorders seem

(1) to be more easily conditioned to fear stimuli,

(2) to sustain conditioned fears longer, and

(3) to respond more strongly to unpredictable threats.

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Genetic Influences of Anxiety Disorders

  • a heritability estimate of 0.5 to 0.6 for anxiety disorders

  • genetic vulnerability is tied to higher neuroticism, which in turn predicts the onset of depressive disorders and multiple anxiety disorders

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Neurobiological Correlates: Brain Regions and Activity of Neurotransmitters

  • A set of brain structures is engaged when people feel anxious or fearful- fear circuit

  • important part of this circuit is the amygdala

  • amygdala sends signals to a range of different brain structures involved in processing threat

  • less activity in the medial prefrontal cortex. Helps to regulate amygdala activity—it is involved in extinguishing fears, in conscious processing of anxiety and fear, and in regulation of emotions.

  • link anxiety disorders to disruptions in serotonin levels

  • the size of this early morning rise, called the Cortisol awakening response (CAR), predicted the onset of anxiety disorders over the next 6 years

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