Final Exam Flashcards
Topics: Substance Use Disorder, Psychosis and Schizophrenia, Childhood Disorders, Personality Disorders
What can excessive use of substance lead to?
Dangerous behaviours
Continued use despite persistent problem
What is substance dependence?
Substance abuse resulting in tolerance and/or withdrawal
Define tolerance
Physiological need for increased substance for the same effects
Define withdrawal
Physical symptoms that result from stopping use (e.g., nausea, sweating, tension, headaches, tremors)
What are the stages of substance abuse?
Positive attitude leads to experimentation which leads to regular use then heavy use which leads to physical dependence/abuse
How does the DSM-5 define substance use/alcohol use disorder?
Problematic pattern of ETOH use leads to impairment
How does the DSM-5 diagnose substance use/alcohol use disorder?
2+ symptoms within 12 months
More ETOH than planned
Desire to control use
Time spent in ETOH pursuits
Craving
Use leading to interpersonal problems
Use despite above, interpersonal problems
Activities given up because of use
Use in physically dangerous situations
Use despite physical/psychological problems to to ETOH
Tolerance
Withdrawal
What does the WHO describe as harmful alcohol use?
Heavy episodic drinking
≥ 6 drinks
≥ 1x/month
What is the prevalence of harmful drinking patterns?
30% Canadian undergraduates vs 17% of the population
People who use a lot of alcohol in university does not mean they will continue to do so in adulthood
What is BAC and what affects it?
Amount ingested in a particular period of time
Food eaten, sex, age, medications
What are some short-term effects of heavy alcohol use?
Stimulating, then depressant action
Interference with complex thought and motor coordination
Interacts with several neural systems
Effects strongly tied to expectations
How does heavy alcohol use interact with neural systems in short-term use?
Stimulates GABA receptors (tension and motor coordination goes down)
Increases 5-HT and DA (motivation for pleasure/craving, addictive)
Inhibits glutamate receptors (cognitive effects)
Biopsychosocial model of Substance Use: Etiology: Bio
Genes
Alcohol risk personality
Ability to tolerate/metabolize alcohol
Motivation for substance use (decrease tension vs increase pleasure)
Biopsychosocial model of Substance Use: Etiology: Psycho
Stress, tension reduction, (negative) reinforcement
Expectations of social success
Perceived benefits outweigh the costs
Sensation (novelty) seeking
Drinking motives
What are the drinking motives?
Positive Internal: Enhancement (highest risk)
Sensation seeking
I am feeling great
Negative Internal: Coping (highest risk)
Stress, tension reduction, reinforcement
How do I deal with this?
Positive External: Social
Expectations of social success
I want to enjoy people more
Negative External: Conformity
Perceived benefits outweigh costs
I don’t want to be judged so I am going to do it to fit in
Most common at highschool and university age
Biopsychosocial model of Substance Use: Etiology: Social
Culture
What you see is what you do
Attitudes/use patterns
Tradition of aggression
Religion
Family
Parent use/guidance
Family/marital problems
Older siblings
Exposure and learning
Availability of substance
Peer/social influences
Media
Biopsychosocial model of Substance Use: Treatment: Bio
Medication: block desire to drink (operant conditioning)
e.g., Antabuse, naltrexone
Lower side effects of withdrawal (e.g., valium)
Transtheoretical Model (TTM)
What are the 6 stages of change in the transtheoretical model?
Pre-contemplation: no mention of changing behavior
Contemplation: start thinking about change
Preparation: intend to take action
Action: start making changes and developing new behavior
Maintenance: sustaining changes and developing new behavior
Relapse: return to old ways (common)
Biopsychosocial model of Substance Use: Treatment: Psycho
CBT and Behavioural
Aversion conditioning
Skills training
Self-control
Motivation enhancement
Controlled drinking vs abstinence
Biopsychosocial model of Substance Use: Treatment: Social
Group therapy
Forced to confront problem
Alcoholics Anonymous (AA)
Environmental intervention (e.g., halfway houses)
What is the treatment efficacy for substance use?
Wide range
Depends on everity of substance abuse (duration, amount of tolerance), and type of treatment
All treatment types are equally effective
List drugs that are associated with addiction
Narcotics
Sedatives
Stimulants
Includes ADHD meds
Anti-anxiety drugs
Pain medication
Hallucinogens
What are some short term biological effects of opioids?
Decreased physical pain
Relaxation
Decreased anxiety
Euphoria
What are some long term biological effects of opioids?
Physiological craving
Withdrawal symptoms
Physical deterioration
Immune system, organ damage
Consequences of poor health, dangerous behavior
Explain the DA theory of addiction
Addiction = dysfunction of DA reward pathway
Drugs lead to heavy dopamine dump which leads to no dopamine for normal activities
All addiction comes from motivation for pleasure
Explain reward deficiency syndrome
Addiction = genetic deviation in reward pathway
Less satisfaction from natural rewards are more likely to become addicted once exposed
What is comorbidity of opioid abuse?
70% other psychological disorders
50% other substance abuse
36% history of trauma
Depression
Anxiety
Antisocial personality disorder
What are different types of stimulants?
ADHD meds
Cocaine
Amphetamines (meth)
Caffeine
Nicotine
What are symptoms of amphetamine abuse?
Intense fatigue
Psychological and physically addictive
Brain damage, amphetamine psychosis
Suicde, homicide, violence
Highly activating
What are different types of hallucinogens?
LSD
Mescaline
Psilocybin
MDMA (ecstasy, molly)
What are some short-term effects of MDMA use?
Rush of pleasure
Sense of wellbeing
Depressed mood (for days after use)
What are some long-term effects of MDMA use?
Brain damage (frontal and temporal lobes)
Memory deficits
Hallucinations
What are some short-term effects of cannabis use?
Relaxation, sense of wellbeing, euphoria `
Hallucination
Increased perceptual acuity
What are some therapeutic effects of cannabis use?
Decrease nausea and pain
Increase appetite and sleep
What are some long-term effects of cannabis use?
Psychosis/schizophrenia (if have the diathesis)
Memory loss
What is psychosis?
Significant loss of contact with reality
Hallmark of schizophrenia
Delusions
Hallucinations
Disorganized speech and/or behaviour
What is schizophrenia?
Disorder characterized by major disturbances in thought, emotion, and behaviour
Disordered thinking
Flat emotions or in appropriate reactions
Highly unusual motor activity
What are the hallmark symptoms of schizophrenia?
Delusions
Hallucinations
Disorganized speech and/or behaviour
*have to have at least 2
What’s the difference between positive and negative schizophrenia symptoms?
Positive: Excess or distortion in typical range of behaviour and perception (more, added on)
Negative: Deficit of typically present behaviours, reduced expressive behaviour, reduced motivation/pleasure (taken away)
*Usually get more negative symptoms the older you get/farther along in diagnosis
Describe delusions
Erroneous (incorrect) beliefs
Highly unusual thought content
Firmly held belief despite evidence
Examples:
Thought insertion
Broadcast thoughts
Thought withdrawal
Made feelings
Describe hallucinations
Sensory experience (any sensory modality)
Seems real despite no external stimulus
Examples:
Voices talking about person
Unusual images
Sensations of things crawling on skin
Describe disorganized speech/behaviour
Speech:
Context - grammatically correct form, but does not make sense (loose associations)
Form - grammatically incorrect (clang association)
Behavior:
Catatonia
Unusual complex movements
Waxy flexibility (immobile posture)
What were the positive and negative symptoms from the in class case study?
Positive symptoms:
Delusions (grandiose, persecutory)
Ideas of reference
Disorganized thinking
Negative symptoms:
Blunted affect
Asociality
Anhedonia
What is the typical age of onset/life expectancy for schizophrenia?
18-30
Shorter life expectancy
Increased risk for suicide
20-40% attempt suicide
105 complete suicide
What are the 3 phases of schizophrenia?
- Prodromal:
Obvious deterioration in role functioning
Personality change (schizotypal PD) - Active:
Psychosis - Residual:
Improvement in positive symptoms
Continued negative symptoms
What are some risk factors/affecting factors towards schizophrenia?
Conceived with a dad over 50
Parents in dry cleaning business
Severity: males > females
Age of onset (younger = more severe)
Premorbid functioning
Cognitive ability
Access to treatment (3-5 years)
Biopsychosocial model of Schizophrenia: Etiology: Bio
Most important ~ 80%
Environment affects expression of symptoms
Genetic markers
Brain structure and function
Original vs revised DA hypothesis
Dopaminergic pathways
Glutamate hypothesis
Neurodevelopment hypothesis
Later environment stressor
Multiple HIT model
Explain genetic markers in regards to the development of schizophrenia
Identical twins have a 50% risk of both having it which means there is an environmental piece to it
Can be a biological environment
Behavioral markers
Smooth-pursuit eye movement
Tracking deficits
People with SCZ and relatives
Explain brain structure and function in regards to the development of schizophrenia
Pyramid
Decreased brain volume
Enlarged ventricles
Reduced volume of the thalamus
Abnormalities in the temporal lobe areas
Hypofrontality
Temporal cortex, language areas
Describe the stages in the brain structure and function pyramid from bottom to top
Disorganized cytoarchitecture:
Cells line up with each other but with schizophrenia they tend to not have as uniformed of a structure
Disrupted brain development in adolescence:
Things are going wonky
Loss of gray matter:
Cell bodies are dying, neurodegeneration
Loss of white body:
Fewer connections
Attentional and working memory deficits:
As the cells start deteriorating it is much harder for them to get their jobs done
Impaired social cognition:
Not understanding what is happening socially
What effect does reduced volume of the thalamus have?
Gateway for processing all incoming sensory info
Call center director
Relays information less effectively, can’t understand
Likely due to disorganized (difficulty with) perception and thoughts
What effect does hypofrontality have ?
Reduced neural connectivity
Excessive synaptic pruning (use it or lose it)
Major DA pathway (PFC inhibits DA in limbic system)
Working memory
Representing sensory info to guide behavior
Disorganized behavior and speech, thought disorder
What effect does the temporal cortex have?
Broca’s area: speech production
Wernicke’s area: language comprehension
Broca’s area is active during an auditory hallucination since it is producing the voice
Explain original DA hypothesis in regards to the development of schizophrenia
Schizophrenia ↔ DA excess
Drugs ↑ DA
Result in schizophrenia like behavior
E.g., amphetamine, L-Dopa for Parkinson’s disease
Drugs ↓ DA
Reduce schizophrenia like behavior
E.g., neuroleptics
Do not treat negative symptoms
*Drugs that increase DA increase schizophrenia and drugs that decrease DA decrease schizophrenia
Explain revised DA hypothesis in regards to the development of schizophrenia
Negative symptoms
↓ DA in cortical regions
Underactivity at D1 receptors
Positive symptoms
↑ in DA subcortical regions
Pre synaptic
Too much produced and released into synapse → overactivity at D2 receptors
Post synaptic
Some findings of too many D2 receptors
What’s the primary difference between the original and revised DA hypotheses?
The original believes the too much DA increases schizophrenia where too little decreases it but only in regards to positive symptoms
The revised accounts for both positive and negative symptoms
Explain dopaminergic pathways in regards to the development of schizophrenia
Mesolimbic pathways (positive symptoms)
Nucleus accumbens (NA)
Ventral tegmental area (VTA)
Where a ton of the DA is produced and it is sending it to the NA
Excess activity here in positive symptoms
Mesolimbic pathways (negative symptoms)
The VTA sends DA to the frontal cortex and when there is more DA there it the limbic system can’t tell it to stop
Both pathways are reversed
Explain glutamate hypothesis in regards to the development of schizophrenia
↓ Glutamate
PCP and ketamine → schizophrenia like behavior
Underactivity at NMDA receptors
DA receptors also inhibit glutamate activity so too ↑ DA activity leads to too ↓ glutamate activity which increases schizophrenia symptoms
Glutamate plays a role in learning, memory, neural processing
Explains problems with attention, working memory, excessive function
Explain neurodevelopment hypothesis in regards to the development of schizophrenia
Silent lesion
Neuromotor, cognitive and behavioral abnormalities:
Smaller head circumference at birth
Slower to reach developmental milestones
Higher rates of left-handedness
Congenital minor physical and craniofacial anomalies:
Velocardiofacial syndrome
Gestational and perinatal exposures:
Viral infection
Early nutritional deficiencies and maternal stress
Pregnancy and birth complications
Maternal starvation (1st trimester
Hypoxia (less oxygen)
Maternal viral infections
Explain the silent lesion hypothesis
Abnormalities lie dormant until normal developmental processes expose problems
Brain makes up for the loss and in adulthood you realize you are missing a piece
Related to prefrontal cortex development
Problems in the neural system are present way before you actually see the symptoms
Explain later environmental stressor in regards to the development of schizophrenia
People with schizophrenia are 2x as likely as the general population to smoke cannabis
An extensive study found if people consumed a lot of weed at the age of 14 that increased risk later in life
Could be caused from cell death due to weed
Diathesis-stress
COMT gene
Breaks down proteins
What relationship do COMT alleles have to risk of schizophrenia and weed usage?
Met → high DA
There is no difference in schizophrenia development if you use weed in adolescents with 2 met genes
Val → lower DA
People with one met and one val gene have a increased risk of schizophrenia if they consume weed and a very low risk if they do not
Biopsychosocial model of Schizophrenia: Etiology: Psychosocial
Multiple HIT model
Psychological stress
Increased relapse rate
Migration: 2nd generation migrants have double the risk than 1st generation migrants
Urbanization
Lowest SES
Sociogenic hypothesis
Social selection theory (downward drift)
From developing vs developed countries: 3.3
From areas with predominantly black population: 4.8
Family
Outdated - schizophrenogenic mother
Current - expressed emotion - relapse much more
Criticism
Hostility
Emotional over-involvement
Explain multiple HIT model in regards to the development of schizophrenia
Brain development from conception to early adulthood
How are cells are forming
Anatomical and functional disruption in neuronal connectivity and communication
Cognitive dysmetria (dysregulation of information processing in the brain)
Impairments in higher-order cognitive processes (e.g., attention, memory, language, emotion)
Symptoms of schizophrenia (e.g., hallucinations, delusions, negative symptoms, disorganized speech)
Biopsychosocial model of Schizophrenia: Treatment: Response
33% continue to have symptoms and problems even after treatment
12% need long term institutional care
38% function well 15-25 years later (can manage symptoms)
10-15% fully recover
Symptoms remit > 2 years, good social functioning
No cure
Biopsychosocial model of Schizophrenia: Treatment: Bio
Historical:
Prefrontal lobotomy
Institutionalization
Insulin coma
ECT
Current:
Antipsychotic medication
Mechanism: block DA receptors
1st generation (more complications/side effects):
Conventional antipsychotics
2nd generation:
Atypical antipsychotics
*Need the meds
What is the range of response for schizophrenia treatment?
1+ psychotic episodes:
Episode has relatively rapid return to normal functioning
Good prospects for recovery
Years of recurrent psychotic relapses:
Periods of remission
Varying degrees of residual impairment
Failure to respond
Biopsychosocial model of Schizophrenia: Treatment: Psycho
CBT:
Create space for consideration that what they are experiencing may not be true
Reframe positive symptoms
Identify triggers for symptoms
Improve social skills
Reduce relapse (not helpful for negative symptoms)
Cognitive remediation:
Improve cognitive functioning
Other individual:
CBT + life skills
Biopsychosocial model of Schizophrenia: Treatment: Social
Family therapy
Communication skills
Decreased expressed emotion
Case management
Social and living skills training
Vocational rehabilitation
What is developmental psychopathology?
How childhood disorders are discussed
Some sort of maladaptation (biological, psychological, and/or socially) happening over the course of typical development
Origins and course of individual maladaptation in context of typical growth process
What is the epidemiology of childhood disorders
~15%
Anxiety is more common
Likely underestimate since often don’t line up with diagnostic criteria
Half (most) have more than 1 disorders
25% (very few) get treatment
Treatments have long wait times
What is the median onset ages for different childhood disorders?
6 - anxiety
11 - behavioural
13 - mood
15 - substance use
What are the most common mental health problems in children?
Anxiety, irrational fears
Depression
Aggression, rule violation
*Attention deficit/hyperactivity disorder (ADHD)
What are common questions regarding childhood disorders?
How is functioning different?
How might differences influence disorders thinking and behavior?
How are children more vulnerable to developing psychopathology?
Biopsychosocial model of Childhood Disorders: Etiology/presentation: Bio
Brain:
Incomplete development of the PFC (the brakes) leaves amygdala (the gas) unchecked
Difficulty stopping when impulse takes control
Aggression, fear, lack of impulse control
Leaves the functioning to make one more likely to behave in certain ways
Ability to control plan and stop ourselves
Real loud in childhood
Engage in unhealthy behavioral habits
Synaptic pruning :
What you practice is what you keep
Automatic cognitions → strong connections
Childhood views shape your adulthood views
Biopsychosocial model of Childhood Disorders: Etiology/presentation: Psycho
Lack of experience:
Do not have the resources to rely on to change attributions
Theory of mind:
Not knowing how everyone sees things
What I think is how everyone thinks
Self = cause of others behaviors:
Believing oneself is the center of everything
Could be related to narcissism
Simplistic view of self/world:
Black and white
Not seeing the contexts of things
Immediate threats seem very important:
Threat is life ending
Biopsychosocial model of Childhood Disorders: Etiology/presentation: Social
Relationships
Dependence on others
For survival
Lack of control over environment
Level of stress in environment
Maltreatment
235000 reported investigations (2003)
½ substantiated
Agreed that it happened
Most abuse does not have evidence
Increase odds of developing psychological disorder
Causal
Do not have to have the gene to develop
Biopsychosocial model of Childhood Disorders: Treatment
Evidence based treatments
CBT
IPT
Family systems
Other common treatments
Psychodynamic therapy
Play therapy
Standard
More value in using as an assessment tool vs treatment
What are issues for treatment in childhood disorders?
Child can’t seek treatment
Adults can get kids into treatment
Early intervention
Kids don’t know the help that they need
Need to treat parents/family
Family and parents can have a lot of influence on how treatment goes
Can continue lessons in the home
Counteracting treatments
Not changing behavior
Shift the way the parent acts can shape the environment the child is in
How are anxiety and depression related in childhood?
Internalizing disorders
High comorbidity:
Anxiety often develops first, which then causes depression to emerge
As you start to avoid things, there is less meaning in life which often leads to depression
Environmental triggers
Anxiety: threat, risk
Depression: loss, high and chronic stress
Learned helplessness
What is the epidemiology of anxiety and depression in childhood?
~6% of children (ages 5-17)
High comorbidity among anxiety disorders
Girl > boys (2:1)
Boys are more likely to display behavioral/disruptive behaviors
Genes
Temperament: behavioral inhibition
Tendency to avoid novel and unfamiliar situations (e.g., toys, people)
Difference in autonomic (sympathetic nervous system) reactivity
More easily conditioned to anxiety
Biopsychosocial model of Childhood Anxiety: Etiology: Social
Early relationships
Higher anxiety and lower adaptive coping skills
Parents : anxiety sensitizers vs suppressors
E.g., a child wakes up
Parent helicopters and treat them like a fragile kid
Parent who teaches them skills to cope with the feelings
Environment
Unusual level of stress, threat, exposure
E.g., dangerous neighborhood, war/bombings, maltreatment
Biopsychosocial model of Childhood: Treatment: Bio
Bio
SSRIs (+CBT)
Biopsychosocial model of Childhood Anxiety: Treatment: Psychosocial
Behavioral therapy
Child CBT + parent/family treatment
2x effective as child alone
E.g., parent-child interaction therapy
CBT skill
Problem solving, finding a whole bunch of solutions
Identify numerous solutions
Adult supports child to solve herself
What are the problem solving STEPS?
Situation
Think of the possible solutions
Evaluate the solutions
Pick one
See if it worked
What is the epidemiology of childhood depression?
Age:
Preschool (1%)
Grade school (2-4%)
Adolescence (8-15%)
Sex:
Childhood - approximately equal
Adolescence - girls > boys = 2:1
Course:
Average MDE 7-9 months
Average 2 years, 90% recovered
Recurrent
Biopsychosocial model of Childhood Depression: Etiology: Psycho
Same as adults
Perfectionism
Super rewarded to be good
Stifles people because they have a fear of failure
Biopsychosocial model of Childhood Depression: Etiology: Social
Depressed parent
2-3x more depression
15% to 45% lifetime risk
Critical parent
Particularly important
More critical more hopeless
Others same as for adults
Biopsychosocial model of Childhood Depression: Presentation: Psycho
Formal operations
Abstract, complex thoughts
Egocentrism
Cognitive inflexibility
Metacognition
How I am as a person
Beliefs about themselves
Children:
Somatic complaints, psychomotor retardation
Physioal
Slower movement, speech, thinking
Greater overlap with anxiety
Adolescence:
Hopelessness, hypersomnia, weight changes
Depression and suicide:
Ages 12-17: second leading cause of death
Ages 5-14: fifth leading cause of death
Biopsychosocial model of Childhood Depression: Treatment: Bio
SSRIs
Can increase suicide risk in youth
Side effects
Family history
Biopsychosocial model of Childhood Depression: Treatment: Psycho
CBT
Behavioral activation
Increase mastery
Biopsychosocial model of Childhood Depression: Treatment: Social
Interpersonal therapy
Parent child relationship
Getting them to react differently
Ways to connect with people
What is the epidemiology of ADHD in childhood?
1-7% of population
Increasing in past 5 years
4:1 boys : girls
60% persistent (ADHD as adults)
Mild hyperactivity symptoms that may grow out of
What is the difference in how ADHD presents itself between girls and boys?
Girls tend to be compliant
Boys tend to be problematic
ADHD usually leads to other disorders
What are the childhood ADHD subtypes in the DSM?
Inattentive
Hyperactive-impulsive
Combination
What are the childhood ADHD DSM symptoms?
Hyperactivity
Forgetfulness
Poor impulse control
Distractibility
Run by a motor
What are Russell Barkley’s reconsidered symptoms of ADHD?
ADHD is a disorder of:
Self regulation
Executive function
Presentation:
Issue is performance (not skill)
Low response inhibition
Time blindness
Periods of hyper focus (DA)
Difficulty with transitions
What is the nature of ADHD?
Chronic neurological “disorder”
Variety of treatments to manage symptoms
Also benefits of ADHD
Calmer feeling during crisis
Biopsychosocial model of Childhood ADHD: Etiology: Bio
Genes
>30% have family members with ADHD
NTs
Low DA
Much more likelihood of getting into trouble (sensation seeker)
Pre-perinatal stress
Cocaine use
Birth complications
Really its genetic
Biopsychosocial model of Childhood ADHD: Etiology: Psychosocial
Not much
Family adversity and disorganization (weak correlation)
Biopsychosocial model of Childhood ADHD: Presentation: Bio
Hyperactivity-impulse control:
Poor connections between amygdala and PFC (impulse control)
Underactive Behavioural Inhibition System (BIS)
Under arousal theory
Inconsistent attention:
Striatum + frontal lobes + posterior periventricular region (controlling and directing attention)
Interconnected with sensory cortices
Act as a gate
Important information registers
Irrelevant noise filtered out
They are underactive so there is attention everywhere, very open to stimuli
Sensory cortices flooded with incoming messages which lead to high blood flow
Biopsychosocial model of Childhood ADHD: Treatment: Bio
Medication is most effective in managing symptoms
Methylphenidate (ritalin, concerta):
Redistributes blood flow in brain
Increases function of striatum, frontal lobes, and posterior periventricular region
Increase availability of DA
Increased focus, inhibitory control, regulation of extraneous motor behaviour (e.g., fidgeting)
Reduce symptoms of in 60-80% of school age children
Biopsychosocial model of Childhood ADHD: Treatment: Psychosocial
Cognitive:
Externalize executive functioning (schedule, reminders)
Behavioural:
Reward systems, frequent breaks
Environmental adjustment and accommodation necessary
Behavioral parent (and teacher) training
Behavioural programs emphasizing:
Time-limited attention, emotion regulation, and rule following
What is conduct disorder?
Baby antisocial personality disorder
Violation of rules and disregard for basic rights of others
Aggression to people and animals
Destruction of property
Deceitfulness or theft
Serious violation of rules
Lack of remorse
What is the epidemiology of conduct disorder?
Comorbidity
ADHD (likely based on emotion dysregulation or arousal seeking)
Substance use
Anxiety and depression (common)
Prevalence (ages 4-16)
8% of boys
3% of girls
Course
Childhood onset: boys > girls
Life course persistent (sticking around, traits)
Adolescent onset: boys = girls
Adolescence limites (maturity gap)
Biopsychosocial model of Childhood Conduct Disorder: Etiology: Bio
Genes:
50% heritability (antisocial behavior)
MAOA gene - the warrior gene
Breaks down 5-HT, SE, DA when you do not have this gene you tend to be more aggressive
Gene x environment correlations:
Passive rGEs (parent created) that is more likely for the kid to behave in certain ways
Active rGEs (kid created) they are going to seek out certain environments
Callous-unemotional style
Executive dysfunction
Poor problem solving and planning that leads to poorly thought out, maladaptive reactions to distress and conflict
Biopsychosocial model of Childhood Conduct Disorder: Etiology: Psycho
High emotional reactivity
Sensation seeking
Chronic underarousal which leads to stimulus seeking
Empathy and perspective taking deficits
Hostile attributional bias
Biopsychosocial model of Childhood Conduct Disorder: Etiology: Social
Modeling
Inter parent discord
Overly harsh discipline (worse things tend to get)
Inconsistent contingencies (e.g., based on mood) in how people parent do not make sense to the kid
Low involvement, weak bonding , poor monitoring
Differential attending/rewarding (coercive process)
Biopsychosocial model of Childhood Conduct Disorder: Treatment: Bio
Antipsychotics
Stimulant medication
Biopsychosocial model of Childhood Conduct Disorder: Treatment: Social
Harsh discipline increased delinquency
Family intervention (fundamental piece)
Parent management training
Multisystemic treatment (MST)
Involves child, family, school, peer group
Often used instead of incarceration
How does parent management training work?
Relationship-building (1:1 time)
Attending (and active ignoring things like swearing)
Effective instructions
Praise and reward system (shaping)
Consequences (privilege removal, removing attention)
What is multisystemic treatment (MST)?
Aspects of
CBT, case management, family systems treatment
Fit between problem and systemic context
Encourage responsible behavior in family members
Require daily/weekly effort from family
What is the pattern of behaviour of personality disorders?
*In DSM-5, must be over 18
Chronic (throughout life):
Early onset (childhood or adolescence)
Stable and longstanding
Pervasive across life areas
Identity (central to the person’s identity):
Inflexible
Deviate from cultural expectations
Clinical distress or impaired functioning:
Cognition (thinking)
Affect (emotions)
Interpersonal functioning
Impulse control
Explain cluster A personality disorders
Paranoid: suspicious, mistrustful, expect attacks
Schizoid: inability to form attachments (and no interest)
Schizotypal: strange (often magical) thinking; perception and speech interferences with communication
Overall characteristics: odd, eccentric, avoid social contact
Explain cluster B personality type
Antisocial: disregard and violation of others rights, serious violation of social norms; deceitful, manipulative; conduct disorder in childhood
Histrionic: dramatic, (mainly sexual) attention seeking (temper outbursts if cannot achieve); emphasis on attractiveness
More common in women
Borderline: impulsive; extreme emotional reactivity; drastic mood shifts; self-injury/suicicde attempts
Narcissistic: grandiosity; attention seeking; lack of empathy; self promoting
Overall characteristics: dramatic, erratic, punitive, hostile
Explain cluster C personality type
Avoidant: shy, hypersensitive to rejection, extreme social insecurity, self conscious and self critical
Dependent: extreme discomfort being alone; suppress own needs to keep relationships; indecision
Obsessive-compulsive: excessive concern with order, rules, and trivial details; rigidity; perfectionism; lack of warmth
Overall characteristics: anxious, fearfulness
What is the prevalence of personality disorders?
10-12% meet criteria for more than 1 personality disorder
Cluster A: ~4
Cluster B: ~4%
Cluster C: ~7%
What are some difficulties in studying personality disorders?
Criteria is not sharply defined
Categories are not mutually exclusive
Personality characteristics are dimensional (what’s the cutoff)
Lack of agreement on assessment measures
What are the categories in the 5 factor model?
Openness: openness to experience (feelings, ideas, actions, ideas)
Conscientiousness: order, duty, achievement, self-discipline
Extraversion: warmth, excitement seeking, positive emotions
Agreeableness: trust, compliance, altruism
Neuroticism; anxiety, anger-hostility, depression, self consciousness
What makes personality disorders difficult to treat?
Varied goals
People aren’t open to treatment
Clients belief in need to change
Client response
Relationships are hard to develop
Cilnican motivation and patience
37% (alot) drop out early, since there is not immediate results
What are the main characteristics of borderline personality disorder?
Impulsivity:
Impulsive reaction to dysphoria/distress leads to self-injury, substance abuses, etc.
Affective instability:
Rapid mood changes (often mistaken for bipolar disorder)
What are the differences between BPD and bipolar?
BPD:
Dysthymic and emptiness
Anger and anxiety
Highly responsive to environmental changes
Minutes to hours (based on what’s happening)
Bipolar disorder
Neutral
Depends on phases in cycle
Weeks to months
What are the domains and symptoms of dysregulation?
Emotional:
High emotional reactivity
Unstable mood (depression, anxiety, irritability, anger)
Interpersonal:
Rejection sensitivity is the underlying driver
Fears of abandonment
Unstable and intense relationships
Behavioral:
Extreme impulsivity related to intense emotion
NSSI, suicidal behavior
Self:
Feelings of emptiness
Unstable sense of self
Stress related paranoia/dissociation
What is the course of BPD?
Young adulthood there is greater impairment and suicide risk but as they get older there is more stability
Over half of people with BPD do not meet full criteria 10 years later even without treatment
It is not stable
What is the prevalence of BPD?
1-2% of population
High among psychiatric inpatients (20%)
Women = men (show different behavioral patterns)
What is the comorbidity of BPD?
Mood disorders (85%)
Anxiety disorders (83%)
Substance use (78%)
Eating disorders
PTSD
Other cluster B personality disorders
*Very likely to have more than one
Biopsychosocial model of Borderline Personality Disorder: Etiology: Bio
Traits (negative emotional responsiveness):
Neuroticism
Impulsivity
5x more common among first degree relatives
Relatives - impulse spectrum disorders (e.g., ASPD, substance abuse)
Biopsychosocial model of Borderline Personality Disorder: Etiology/Presentation: Bio
Decreased orbitofrontal volume which leads to impulsivity, aggression, mood instability
Decreased hippocampal volume which leads to stress overreactivity (anxiety), increased fear responses
Amygdala hyperactivity, easier conditioning to fear, affective lability
Lower 5-HT leads to impulse behavior, disinhibition
How is amygdala hyperactivity related to BPD?
Hypervigilance
Emotional dysregulation
Neutral = threatening
Biopsychosocial model of Borderline Personality Disorder: Etiology/Presentation: Psycho
Emotion
Perceived rejection leads to intense rage (fight)
Misperception of anger, usually is actually fear
Cognition
Thinking mistakes
Black and white thinking, catastrophizing (similar to anxiety and depression)
Result of fear of abandonment and rejection
Biopsychosocial model of Borderline Personality Disorder: Etiology: Social
Invalidating environment
Early adverse events
Trauma/maltreatment (8x higher risk for cluster B)
90% childhood physical, sexual abuse, and/or neglect
Early separation or loss (lack of safety)
Abnormal parenting
Bonding
Neglectful and overprotective
What is the biosocial theory?
Diathesis to stress
Biological diathesis for emotional reactivity plus invalidating environment leads to BPD
Invalidating environment:
Efforts to communicate inner experience disrespected or punished (being shut down)
Child suppresses emotions leads to explosion to get parents attention which reinforces the outburst
Biopsychosocial model of Borderline Personality Disorder: Treatment: Bio
Comorbid mood disorders:
SSRIs
Mood stabilizers
Psychotic/dissociative symptoms
Antipsychotics
Biopsychosocial model of Borderline Personality Disorder: Treatment: Psycho
Dialectical behavior therapy (DBT):
Intensive (2 sessions a week, diary cards daily, for a year )
Expensive
Mentalization:
Client-therapist relationship
Perspective taking, cognitive flexibility
Transference-based psychodynamic psychotherapy:
Client-therapist relationship
Expensive
Takes years
What are the DBT principles?
Acceptance:
ACT
Validation, why are you doing what you’re doing
Change:
CBT
Problem solving
Dialectics:
Balancing the two
What are the assumptions of DBT?
Acceptance:
Individuals are doing the best they can
They want to improve
Change:
At the same time;
They need to do better, try harder, be more motivated to change
They may not have caused all of their problems; they have to solve them anyway
Their lives are often unbearable as they are currently being lived
They must learn new behaviors in many contexts
What is the format of DBT?
Individual therapy
Skills group:
Mindfulness (awareness and attention)
Emotional regulation
Distress tolerance
Interpersonal effectiveness
Dialectics (walking the middle path)
What are the main characteristics of antisocial personality disorder?
Inadequate conscience development
Ability to impress and exploit others
Irresponsible and impulsive behavior
What are the symptoms of ASPD?
Disregard for and violation of the rights of others
Deceitfulness
Impulsivity
Aggressiveness
Reckless disregard for safety of self or others
Consistent irresponsibility
Lack of remorse
*Don’t have to have all, have to have some
What is the comorbidity of ASPD?
Substance abuse
Other cluster B personality disorders
What is the prevalence of ASPD?
Community:
3% men
1% women
Prison:
47% (half) men
21% (some) women
Younger adults
Lower SES
Biopsychosocial model of Antisocial Personality Disorder: Etiology: Bio
PFC dysfunction:
Poor executive control
Genes:
Low MAOA (warrior gene)
Enzyme that breaks down 5-HT, NE, DA
Structural and functional changes in brain
On X chromosome
Traits:
Aggressiveness
Impulsivity
Low anxiety
Biopsychosocial model of Antisocial Personality Disorder: Etiology: Psychosocial
Low income
Low parental supervision
Parent psychopathology
Delinquent sibling/papers
Neglect
Abuse (physical or sexual)
Harsh discipline
Explain the course of ASPD
Strong risk
ODD (age 6) leads to conduct disorder (age 9) leads to ASPD
ADHD + CD leads to ASPD (possibly psychopathy
What is the difference between ASPD and psychopathy?
ASPD:
Broader category
More behavioural symptoms (criminality)
Psychopathy:
Narrow
Personality structure
Born this way
Developmental risk factors
ASPD:
Difficulty learning to regulate emotions
High emotional reactivity (aggressive, antisocial) in response to stress
Psychopathy:
Fearlessness
Low anxiety
Poor conscience
Premeditated aggression
What are the dimensions of psychopathy?
Core:
Interpersonal -
Superficial charm
Pathological lying
Affective -
Lack of remorse, guilt, empathy
Behavior:
Lifestyle -
Need for stimulation, impulsivity
Antisocial -
Poor behavioral control
Criminality
Biopsychosocial model of Antisocial Psychopathy: Etiology: Bio
Genes:
~50% variance
Callous/unemotional traits (heritable)
Brain structure:
Amygdala volume (more often in unsuccessful psychopathy)
Brain function:
PFC dysfunction (more often in unsuccessful psychopathy)
Biopsychosocial model of Antisocial Psychopathy: Etiology/Presentation: Psycho
Callous/unemotional traits
Low levels of fear/poor conditioning of fear (opposite of BPD)
Cognitive encoding, don’t encode things as dangerous
Low physiological and emotional encoding
High reward sensitivity
Attentional directedness (tunnel vision)
Biopsychosocial model of Antisocial Psychopathy: Etiology: Social
Early parental loss
Parental loss or rejection
Callous/unemotional traits evoke negative negative parenting responses:
Anger
Frustration
Harsh discipline
Biopsychosocial model of Antisocial Psychopathy: Treatment
Punishment is ineffective
Treatment is very difficult
Early intervention is critical (not completely shut down)
Focus on social skills they get better at manipulating and use other peoples trauma stories
Better to work toward redirecting their skills toward prosocial goals, get them what they want
What does early intervention look like for psychopathy?
If not callous/unemotional:
Reduce
Hostile attributions
Resentment, shame (key element)
Increase
Closeness in relationships
Kind responses to self/others
Lean into softer primary emotions
fear/sadness vs anger/shame
Predict limits
Compassion in caregivers
What is the purpose for laws in psychology?
Rules governing clinicians actions to protect vulnerable persons
Anyone with a disorder is automatically vulnerable
What are the risks in psychology?
Un or under qualified clinicians
Clinicians treating outside areas of expertise
Treatments without empirical support
What are the two local ethic boards?
Canadian Psychological Association (CPA) -
Code of Ethics
College of Health and Care Professionals of BC (CHCPBC) -
Code of Conduct
What are the CPA code of ethics principles?
Respect for the dignity of persons (confidentiality, informed consent)
Responsible caring (clinical competence, treatment must maximize benefit and minimize harm)
Integrity in relationships (unbiased by affiliations, guided only by clinical judgment)
Responsibility to society (recognize how actions affect society, in addition to clients rights)
What are the three legal and ethical issues?
Confidentiality
Involuntray confinement
Deinstilutionalization
What are the important items in psychology?
Guarantee of right and freedoms
No arbitrary detainment or imprisonment
Equality before law
No discrimination
What is the difference between privilege and privacy in confidentiality?
Privlidge:
Right to refuse to disclose information to legal system (in all circumstances)
E.g., lawyer-client communication
Privacy:
Right to choose information being shared (in most circumstances)
E.g., clinician-clinet communication
What does confidential communication mean in clinician-client communication?
Communication is private
Client chooses whether and to whom info can be disclosed (in most circumstances)
Law against breaching confidentiality
What are the expectations to clinician-client confidentiality?
Imminent risk to self or others
Suspected harm to a child or dependent adult (and guardian will not protect)
Driving while intoxicated
Court subpoena
What allows the CPA code to breach confidentiality?
Clinician must breach confidentiality when and 3rd party identifiable victim or class of victims is believed to be at risk
What are some issues in confidentiality?
Clinican efforts to reduce liability:
Asking fewer (important) questions
Vaugue language in session motes so you cannot be held reliable
Who is the client?
Organization vs patient
Parent vs child
Infant act, if you believe the child can consent
What are the 2 types of involuntary confinement?
Criminal commitment
Civil commitment
What is criminal commitment?
Confining person who commits crime due to mental illness to psychiatric institution
What is M’Naughten Rule?
Insanity defense:
Ability to know an act is wrong
Legally not allowed
Morally (standards of society)
Intellectual ability to know right from wrong
Ability to apply that knowledge rationally in the situation (policeman at the elbow), would you be able to stop yourself if there was a cop beside you
What is the irresistible impulse rule (1887)?
Functional
Knowledge of right vs wrong
Nonfunctional
Impulse to act is irresistible
What is neurolaw?
Evidence of disorder neural structure and function = sufficient to alter sentence (held less responsible)
Activation in areas consistent with impulse urges vs inability to control urges
Explain volitional control vs irresistible urges in murderers
Neural systems - checks and balances
Lower self-reflective PFC
More active impulse from amygdala
Impulsive murderers had high subcortical and low PFC, less brain matters
Predatory murderers high subcortical and normal PFC, control and plan
What is civil commitment?
Confining a person to psychiatric institution
No laws broken
Mental illness results:
Dangerous to self or others
Incapable of providing for their basic physical needs
Unable to make responsible decisions about hospitalization
In need of treatment or care in hospital
What are the types of civil commitment?
Informal commitment (no court order)
Formal commitment (court order)
Community commitment (Conditional Treatment Order - CTO)
Explain the dangerousness model
Only to prevent physical harm
Denying personal freedom is serious
Softer standards discriminate against people with mental illness and are paternalistic
Explain the treatment model
Prevent physical harm or serious deterioration
Dangerousness is difficult to predicit
Need to protect vulnerable persons
How do you predict dangerousness?
Strongest predictors:
Psychopathy scores
Elementary school maladjustment score (bias)
Good at predicting:
General recidivism (reoffend)
Sexual and violent recidivism
Extreme violent recidivism
Correlation = .44
What was institutionalization like pre vs post 1960s?
Pre 1960
People with mental disorders were often placed in institutions indefinitely
Post 1960
Massive release of patients to stress
No alternative care provided
Resulted in homelessness, substance addiction, jail
What are Scott Simmie’s potential solutions for deinstitutionalization?
Home care for people with serious mental illness
Community mental health centres as access points
Increase forensic beds
Increase mental health workers in jails
Most effective medications first
Increased early detection and defragment intervention in children
24hr information/crisis line for appropriate referrals
What are André Picard’s potential solutions for deinstitutionalization?
