Studied by 5 peopleCHAPTER 13 Disorders of Childhood
Early life origins of psychopathology
age of onset peaks at teenage years and then another time in adulthood
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
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
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
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.
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
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
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
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.
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.
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)
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
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
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
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
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
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
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%)
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;
Comorbidity is common in conduct disorder. Other problems that co-occur with conduct disorder include_____,,, and____.
ADHD, substance abuse, depression, anxiety
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
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”?
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
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
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?
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?
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
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
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.
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
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
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
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
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
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
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
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
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
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)
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)
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
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
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
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’
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
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?
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?
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
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
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
‘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
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.
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)
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
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
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
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
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”
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
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
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
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
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)
Treatment of specific phobia
Almost exclusively psychological in nature — highly effective
Exposure therapy
In-vivo (real life) exposure
Imaginal exposure
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
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
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
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)
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
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
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
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
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
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
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!
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
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
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
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
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
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
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
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
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)
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
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
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
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
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
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)
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
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
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
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.
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
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
Fear Conditioning in anxiety disorders
Mowrer’s model suggests two steps in the development of an anxiety disorder:
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).
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.
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
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
Note
Flashcard