412 pre-M2 Flashcards

1
Q

10 substances in SUDs

A
  • alcohol
  • cannabis
  • opioids
  • hallucinogens
  • inhalants
  • sedatives and hypnotics
  • anxiolytics
  • tobacco
  • stimulants
  • other/unknown
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2
Q

SUDs diathesis-stress model

A
  • risk-seeking tendencies could act as a diathesis (strong reward neural pathway)
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3
Q

correlates of SUDs

A
  • associated with 3 leading causes of death in adolescents: accidents/injuries, suicide/self-harm, interpersonal violence
  • legal and educational problems
  • comorbidity with other disorders
  • earlier use (14 vs. 21) linked with more substance-related impairment later (risk marker, not causal)
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4
Q

prevalence of substance use and SUDs

A
  • a lot of variability in adolescents, gets more common with age
  • experimentation very common (normative)
  • SUDs roughly 11.4% 13-18 years
  • substance use rates decreased during COVID and remained low
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5
Q

Early brief interventions for SUD

A
  • norm-based interventions for college students (helping people realize how much others are actually drinking - shift toward descriptive norms)
  • large discrepancy between perceptions of peer substance use and what actually happens (overestimating)
  • informing about how much you drink (ranked with peers), your perception of others, and how much your peers drink (shift in perceived norms = changing your behaviour according to the norm)
  • help reduce frequency and quantity of drinking, but not many studies of efficacy in long-term
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6
Q

injunctive norms

A
  • how much others approve/disapprove of a behaviour like drinking
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7
Q

descriptive norms

A
  • how much others are actually engaging in a behaviour like drinking
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8
Q

outpatient treatment for SUDs

A
  • family therapy
  • alcoholics anonymous
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9
Q

family therapy for SUDs

A
  • multidimensional
  • working with caregivers to increase parental monitoring
  • working with teens to improve coping strategies or fix risk-taking behaviour
  • good efficacy (maybe better than CBT)
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10
Q

alcoholics anonymous

A
  • very popular and common worldwide (easily accessible)
  • acknowledge that alcohol is a problem, abstinence is the goal, supported by a peer
  • 12-step program
  • has other equivalents for various drugs (nicotine not as supported)
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11
Q

3 hypotheses in AA

A

(1) attendance itself leads to reduced substance use (meetings help you use less)
(2) lower alcohol use is associated with more AA attendance (less severe = more likely to use AA and more likely to recover)
(3) better prognosis (more motivated, less comorbidity, more protective and less risk factors) = lower alcohol use and benefit from AA

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12
Q

how does evidence support AA

A
  • RCTs show a lack of efficacy (but studies aren’t well done, participants are coerced instead of self-selected into treatment)
  • following Ps who received Tx at a hospital, then attended AA = support for efficacy (lower alcohol use at follow-up)
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13
Q

support for 3 hypotheses of AA

A

(1) AA involvement at 1-year post-treatment predicted lower alcohol use at 2-year post-treatment
(2) alcohol use at year 1 didn’t predict AA involvement at year 2 (people using less don’t attend AA more)
(3) results not explained by AUD severity, comorbidity, or motivation (not a good prognosis that mediates the results)

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14
Q

inpatient treatment for SUDs

A
  • short duration (4-6 weeks)
  • individual counselling, family therapy, treatment for comorbidities
  • often followed by outpatient treatment
  • can get very expensive, especially for teenagers who need multiple stints
  • good rationale (changing the environment and losing access to substances) but very few controlled studies about efficacy
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15
Q

who is least/most likely to use mental health services

A
  • people with severe and non-severe anxiety do not seek treatment (though girls and older adolescents are slightly more likely)
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16
Q

why are people with anxiety less likely to seek treatment

A
  • some fear and anxiety is normal (becoming distressed when separated from parents, short-lived specific fears, must assess if it’s causing distress/disability)
  • some anxiety is adaptive (stranger anxiety, test anxiety)
  • may not be as upsetting to adults (no causing disruption, may be associated with favourable characteristics like less aggression)
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17
Q

core features of anxiety

A
  • focus on threat or danger
  • anxiety is future-oriented (anxious apprehension)
  • strong negative emotion or tension (physical sensations, cognitive shifts like worry, behavioural patterns like avoidance)
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18
Q

different anxiety diagnoses

A
  • vary on content of threat and balance of symptoms (cognitive like worry vs. physical)
  • specific phobia
  • separation anxiety
  • generalized anxiety
  • social anxiety
  • panic disorder
  • agoraphobia
  • selective mutism
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19
Q

epidemiology of separation anxiety

A
  • often seen in school ages
  • high levels of comorbidity (with other anxiety or depressive disorders)
  • small percentage of people will persist into adulthood (figure of attachment may change), while others will grow out of it or switch to another anxiety disorder
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20
Q

selective mutism

A
  • failure to speak in situations when speaking is expected, even though they may speak in other settings
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21
Q

common obsessions and compulsions

A
  • contamination, harm to self or others, symmetry
  • counting, checking, washing
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22
Q

prevalence of anxiety disorders

A
  • any anxiety disorder in childhood/adolescence = 32%
  • specific phobia: 19%
  • social anxiety: 9%
  • separation: 8%
  • GAD: 2%
  • PD: 2%
  • OCD: 1-2%
  • mutism: 0.7%
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23
Q

epidemiology of anxiety disorders

A
  • girls 2:1 boys (as age of onset increases, gender disparity increases)
  • OCD has a 2:1 male to female ratio that is present throughout development
  • contextual cultural experiences can shape anxiety presentation
  • lower SES (single parent, lower parental education) = more anxiety
  • ethnicity: more common in Black youth, but White youth receive more treatment (race-based sensitivity)
  • comorbidity tends to be the norm (with other anxiety disorders and depression)
  • usually, anxiety disorders precede depression (internalizing symptoms are highly related)
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24
Q

race-based sensitivity

A
  • worry/anxiety/physiological arousal about the idea that someone could discriminate against you in the future
  • anticipating people treating you differently because of your race, which contributes to your anxiety
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25
Q

comorbidity anxiety and depression

A
  • symptom overlap (GAD and MDD; fatigue, sleep disturbance, irritability, concentration)
  • negative affectivity high in both anxiety and depression, but depression is low in positive affectivity and anxiety can still have high positive affectivity
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26
Q

clinical correlates of anxiety

A
  • academic difficulties; high IQ but symptoms interfere with functioning (worry impacts concentration, school refusal)
  • social difficulties: becoming increasingly rejected with age because of shyness, more likely to experience peer victimization, perceive their friendships to be of lower quality
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27
Q

developmental course of anxiety disorders

A
  • fears, worries, rituals can be developmentally appropriate (worries get more complex as you age)
  • young children may not realize that their fears/behaviours are excessive/atypical, but may get embarrassed as they age
  • earlier stages of development = inability to verbalize distress, so behavioural symptoms are more common
  • different anxiety disorders have different ages of onset
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28
Q

anxiety disorders age of onset

A
  • separation: 7-8
  • OCD: 9-12 (though some kids can present earlier 6-10)
  • GAD: 10-14
  • social and PD in adolescence
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29
Q

homotypic continuity

A
  • stability
  • a disorder predicts itself over time
  • separation anxiety becomes social anxiety
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30
Q

heterotypic continuity

A
  • disorder predicts onset or worsening of a different disorder over time
  • social anxiety becomes depression
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31
Q

heritability of anxiety

A
  • tendencies toward anxiety are inherited (diathesis)
  • children of parents with anxiety disorders are 5x more likely to have anxiety disorders
  • twin studies indicate 33% of variability is heritable
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32
Q

what could be the inherited biological predisposition for anxiety

A
  • temperament
  • behavioural inhibition: fear and distress in response to novel situations, withdrawal
  • negative emotionality
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33
Q

two-stage model of fear acquisition

A
  • stage 1: develops through classical conditioning (pairing US-CS so that the CS will reliably provoke the CR)
  • stage 2: avoidance behaviour maintains fear through operant conditioning (avoidance = relief = negative reinforcement of avoidance & reinforces the idea that the fear is valid)
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34
Q

maintenance model of OCD

A

obsessive intrusive thought = appraised as important = anxiety and disgust = act to neutralize = reduces distress = reinforcement of important appraisals & more likely to have more intrusive thoughts (because you spent so much cognitive time and energy on them)

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35
Q

social information processing model of anxiety

A
  • encoding biases: attention to threat and reading ambiguous situations as more threatening
  • threat intensity, personal relevance of threat, current mood, contextual factors will moderate attentional biases (not constantly more attentive to threat)
  • interpretation biases: interpreting ambiguous events negatively and catastrophizing mildly negative events which can lead to avoidance
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36
Q

family factors in youth anxiety

A
  • modeling: parents demonstrating anxious responses to children (parent showing fear = child learns to also display fear)
  • information transmission: kids being told that something is dangerous (parents over-emphasizing danger)
  • low expectations: parents not believing that their kids have the ability to cope
  • parental reinforcement of problematic behaviour
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37
Q

study about family factors in youth anxiety

A
  • kids referred for anxiety, ODD, or control group presented with ambiguous situations and give a first answer, then discuss with parents and give a final answer
  • parents talked their kids into giving avoidant responses (maybe they had low expectations about their ability to respond in other ways)
  • direct transmission of information
  • same pattern in kids with ODD: parents socializing and modeling aggressive solutions
  • passive GxE (creating environments that foster anxiety) and evocative GxE (reacting to kid’s anxiety and providing avoidant solutions)
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38
Q

SSRIs

A
  • stop the reuptake of serotonin into the presynaptic neuron
  • some evidence of effectiveness, but not much research in youth
  • reduction of symptoms, moderate effect sizes
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39
Q

core components of effective treatments for anxiety

A
  • reducing cognitive biases by encouraging positive self-talk about anxious symptoms and thoughts that go with them + coping self talk, identifying and challenging automatic thoughts
  • reduce bodily tension though diaphragmatic breathing, progressive muscle relaxation, guided imagery
  • exposure and habituation (facing fears in a controlled way)
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40
Q

novel cognitive interventions for anxiety

A
  • re-training attention threat bias
  • dot-probe task to train attention away from threat (potentially promising)
  • kids assigned to attention-bias modification, neutral-neutral, placebo conditions in a double-blind study
  • only people in the ABM condition showed decreases in threat bias, anxiety severity and symptoms
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41
Q

exposure therapy

A
  • habituating the CS so that anxiety will decrease naturally (without avoidance)
  • CS presented without the US to extinguish the relationship between CS-CR
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42
Q

graded exposure

A
  • start small and work up to higher levels of anxiety
  • develop a hierarchy of fears ranked from easiest to hardest (subjective anxiety)
  • start toward the bottom of the ladder, rate anxiety during each exposure, and keep practicing until habituation to move up the ladder
  • first exposure = strong reaction, then anxiety will decrease so that the next reaction will be lower (peak anxiety will be lower and will decrease faster)
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43
Q

flooding

A
  • can be very effective
  • start with an intense confrontation with the most feared stimulus
  • not very tolerated, so clinicians opt for graded (less likelihood of dropout)
  • if the person cannot tolerate it, so they avoid or fail, they’re unlikely to benefit
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44
Q

CBT for OCD

A
  • normalize OCD and intrusive thoughts (1: psychoeducation)
  • create a hierarchy of obsessions (can get very granular)
  • exposure response prevention
  • teaching to place less importance of intrusive thoughts, limiting compulsions
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45
Q

Child/Adolescent Anxiety Multimodal Study (CAMS)

A
  • testing efficacy of SSRIs, CBT, combined in youth with GAD, separation, social anxiety (treated for 12 weeks, clinician blind ratings of severity)
  • all treatments were better than placebo group
  • combined was better than SSRIs or CBT alone
  • CBT was equal to SSRIs
  • these patterns were maintained at follow-up
  • moderator: anxiety diagnosis (combined was best for all 3, SSRIs were better for social anxiety - maybe taking the edge off, CBT was better for GAD - skills learned might generalize)
  • CBT for SOC didn’t include exposure to peers which could influence the results
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46
Q

CAMELS (Extended Long-term Study)

A
  • 3-11 years post-Tx
  • improvements in functioning (family functioning especially) during CAMS led to long-term improvement in anxiety
  • improvements in anxiety during CAMS led to improvements in functioning
  • patterns were true across all conditions
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47
Q

Pediatric OCD Treatment Study (POTS)

A
  • youth with OCD assigned to SSRIs, placebo, CBT, CBT+SSRI
  • severity rated blindly
  • combined was better than other conditions
  • CBT equivalent to meds
  • effect sizes were different based on the site
  • Duke: combined was better than meds, which was better than CBT
  • Penn: combined and just CBT were equivalent and both better than meds
  • clinicians were better at giving CBT at Penn, and there was no added benefit of giving meds
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48
Q

core features of depression

A
  • dysphoria (prolonged sadness)
  • irritability (excessive sensitivity, hostility, moodiness)
  • anhedonia (loss of pleasure or interest in previously enjoyable activities)
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49
Q

symptom vs. syndrome vs. disorder

A
  • symptom: feeling of emotion or sadness (common)
  • syndrome: cluster of common symptoms (extreme on dimension of negative mood/affect)
  • disorder: syndrome that has been occurring for a certain amount of time and occurring with impairment in functioning
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50
Q

DMDD differential diagnosis

A
  • cannot be diagnosed concurrently with ODD or Bipolar
  • DMDD was created for kids who were being diagnosed with BP but only presenting with irritability
  • DMDD is more chronic irritability, while BP is more phasic
  • more intense irritability than you might see in MDD/PDD
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51
Q

evidence for DMDD

A
  • applying new criteria to existing data = hazy boundaries, not good at identifying those with the disorder
  • DMDD not well differentiated from CD or ODD
  • not much difference in symptom severity or functional impairment with or without the disorder
  • DMDD diagnosis showed poor stability
  • very high comorbidity (also meeting criteria for ODD, which can’t be diagnosed concurrently)
  • validity is questionable, high risk of over-diagnosis (irritability is very common in child development)
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52
Q

epidemiology of DMDD

A
  • limited studies before DSM-5 inclusion showed highest rates of symptoms in preschoolers
  • highest co-occurrence with depressive disorders and ODD, which can’t be diagnosed concurrently (higher rates of social impairment, school suspension, service use, poverty)
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53
Q

categorical vs. dimensional depression

A
  • many kids and teens have subclinical depression
  • still show significant impairment
  • at greater risk for developing depression and other disorders/difficulties
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54
Q

epidemiology of MDD

A
  • 1% or preschool-age kids
  • 2% of elementary-school kids
  • 11% of adolescents
  • racial ethnic differences: Latinx youth and Black youth more likely to experience mood disorders, but white youth more likely to receive Tx (lower SES, discrimination)
  • lack of gender differences in childhood, and divergence increases after 15
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55
Q

possible explanations for the gender gap

A

(1) girls more likely to seek help (gender difference found in community samples, but there isn’t necessarily a difference)
(2) biological factors (onset of gender disaprity emerges during puberty, earlier puberty = depression but only in girls, puberty may sensitize girls to stress)
(3) puberty may create stress for girls (changes in physical appearance, sex-role identification), especially interpersonal stress (peer rejection, conflict, generating stress) because girls are invested in their relationships
(4) cognition: negative attributions (but this appears to be equal for boys and girls)
(5) coping: girls tend to ruminate or co-ruminate

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56
Q

preschool depression

A
  • earlier onset associated with more severe and chronic depression later (and higher rates of ADHD and anxiety at school age)
  • 2-week duration criteria not as relevant for preschoolers (even if not met, still associated with MDD 2 years later)
  • depressed 4-6 year-olds show altered brain activity (more amygdala activity when viewing emotional faces, like you see in adults) - dirupted amygdala functioning could be a biomarker or a consequence of depression throughout lifetime
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57
Q

biological factors for depression

A
  • high (but lots of variability) heritability estimates (35-75%)
  • early exposure to stress can sensitize to later stress (stress reactivity)
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58
Q

stress reactivity in depression

A
  • depression in moms associated with higher cortisol levels which can affect fetus
  • number of months a woman is depressed is associated with child’s elevated cortisol levels at 6-7 years
  • epigenetic transmission of biological processes
  • transmission of altered stress physiology postnatal through breastmilk
  • early experiences (sensitive period) with caregivers important for attachment (maternal depression may be associated with problematic parenting which alters child’s stress reactivity)
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59
Q

social-cognitive processing in depression

A
  • negative encoding biases (attentional, toward sadness/negative affect)
  • interpretation (negative attributional biases, unconscious pattern of response)
  • response search not as important, but still tend to identify fewer assertive responses
  • response decision: report themselves as less able to carry out assertive strategies (and as less effective) and think avoidant strategies are better
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60
Q

interpretation biases study depression

A
  • looking at high-risk population (cognition as a risk factor)
  • blending two words acoustically (neutral-negative, neutral-positive) to make the result a 50-50 chance of hearing either word
  • at-risk girls showed a preference for depression-related negative words (but not threat words), control group showed a preference for positive words
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61
Q

interpersonal theories of depression

A
  • less prosocial, less assertive, more avoidant and withdrawn, kids may be more hostile and aggressive
  • responding to interpersonal challenges in problematic ways
  • difficult to maintain healthy and close friendships with depression (less support, less social skill training)
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62
Q

stress exposure models of depression

A
  • depression caused by exposure to stress
  • peer rejection leads to depression
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63
Q

stress generation models of depression

A
  • higher depression leads to higher stress exposure
  • symptoms impact your interactions, and those difficulties cause interpersonal problems which exacerbate symptoms
  • depressed kids get rejected more
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64
Q

evidence for stress generation models

A
  • clinical interview to place participants into 4 groups: depressed only, externalizing only, both, control
  • assessed life stress experiences and rated them in terms of severity, extent to which child contributed to the event (independent or dependent), interpersonal/non-interpersonal
  • depression associated with dependent and interpersonal stress
  • externalizing associated with dependent and non-interpersonal
  • neither was associated with independent
  • comorbid had highest levels of interpersonal and non-interpersonal
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65
Q

co-rumination

A
  • dwelling on problems without solving them with a friend
  • associated with better friendships, but also with more negative mood
  • dwelling on negative affect with a friend = negative mood, but not friendship quality
  • rehashing the problem and speculating about what might happen = better friendship, but not negative mood
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66
Q

reassurance seeking

A
  • initially, friends are happy to provide reassurance, but people keep seeking because they think they don’t mean it
  • over time, this becomes irritating and invalidating
  • which leads to friendship withdrawal and peer rejection
  • associated with unstable friendships
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67
Q

contagion

A
  • your own depressive symptoms predict your friend’s depressive symptoms
  • co-rumination is the mediating mechanism
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68
Q

CBT model of depression

A
  • based on diathesis-stress model
  • depression maintained through negative cognitive and behavioural processes
  • target depressogenic thinking, low reinforcement and negative life events, skill deficits
  • automatic thoughts and behavioural inhibition
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69
Q

emotional spirals in depression (CBT)

A
  • negative events breed negative moods = negative behaviours = negative thoughts and low expectations for the future
  • spirals can also be positive, so you have to disrupt the negative downward spiral and facilitate positive triggers
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70
Q

cognitive techniques in CBT

A
  • identify automatic thoughts and challenge them
  • bring thoughts in line with the event instead of solely negative or reframing them positively
  • observe thoughts, feelings & behaviour, consider alternative explanations, solve problems rationally
  • orientation toward therapy as an experiment (try something to see if it works)
  • match developmental level (insight and abstract thinking)
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71
Q

behavioural techniques in CBT

A
  • keep track of mood and activity, develop a list of rewarding activities (that produce pride and pleasure)
  • change habits (addressing environmental obstacles and skill deficits)
  • monitor how mood is being affected by these changes
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72
Q

predictors of positive outcomes for CBT

A
  • combined behavioural activation and thought challenging
  • involving parents in the intervention
  • efficacy goes down as severity increases
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73
Q

cultural CBT study

A
  • comparing interventions for depression in non-WEIRD samples
  • CBT, economic, integrated all led to reduced symptoms in low/middle income countries
  • interpersonal trending toward effectiveness, but not reliable yet
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74
Q

antidepressant medications

A
  • much more widely documented in adults, some don’t work at all/less in children (brain development/metabolism differences)
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75
Q

tricyclics

A
  • prevent reuptake of serotonin and NE or increasing responsiveness of receptors
  • not effective in youth
76
Q

monamine oxidase inhibitors

A
  • MAO (enzyme) should break down neurotransmitters, so blocking them will increase their levels in the synapse
  • some mixed evidence of efficacy
  • potentially fatal side effects (tyramine)
77
Q

selective serotonin reuptake inhibitors

A
  • specifically focused on serotonin
  • evidence for fluoxetine efficacy in teens
  • not fatal in overdose
  • some negative side effects
  • takes weeks to work
78
Q

serotonin and norepinephrine reuptake inhibitors

A
  • also block NE
  • still takes weeks to work
79
Q

black-box warning for SSRIs

A
  • suggestion of increased risk of suicide
  • warns of dangerous side effects
  • data from all RCTs using antidepressants showed higher levels of suicidality compared to placebo (no deaths from suicide)
  • other studies show decreased rates of suicidality
  • more recent studies found no association between use of Prozac and higher suicidal ideation in teens
80
Q

media coverage study of suicide and SSRIs

A
  • investigating whether media coverage and warning labels lead to lower use of SSRIs and increased suicide risk
  • looking specifically at psychotropic poisoning (underestimate of SAs)
  • found decreases in prescriptions after the FDA warning
  • found an increase in psychotropic poisonings after the warning
  • no change in completed suicide before and after
81
Q

course of action for using SSRIs for youth

A
  • discuss risk and benefit: could increase risk of suicidal ideation (could increase your energy which makes you more likely to proceed with an attempt)
  • leaving depression untreated can also increase risk of suicide
  • SSRIs are efficacious all around the world for treating depression
82
Q

treating depression in preschoolers

A
  • diagnosis in preschool is still new, so not much data
  • limited data on psychiatric drugs
  • version of parent-management training focusing on helping parents manage their children’s moods
  • helping kids increase positive mood (so there is less room for negative)
  • therapy is first-line, but if it persists, fluoxetine has the best risk-benefit profile (and continuously monitor)
83
Q

Treatment for Adolescents with Depression (TADS)

A
  • at the time of the study, CBT had some evidence but lots of room to improve the treatment, meds were being increasingly used, combined was being used but no idea if this was actually helpful
  • sample was 439 youths with moderate-severe MDD
  • SSRI and combined group did better post-treatment than placebo or CBT alone
  • CBT was most helpful for suicidality (combined and CBT alone groups vs. SSRIs and placebo)
84
Q

explanations for results in TADS

A
  • CBT didn’t outperform a pill placebo
  • CBT might not work in a more severe sample (it worked better in sub-clinical presentations)
  • treatment manual was very flexible (clinicians using different CBT methods, so some participants could have received more helpful skills)
85
Q

TADS follow-up

A
  • after 12 weeks, unblinded placebo and SSRI groups (people who were still depressed in the placebo group received treatment)
  • after 36 weeks from the start (no more control group), all groups were equal
  • could just be time (MDD episodes are cyclical and we don’t have a control group)
  • could be that CBT takes longer to show positive effects
  • 1-year post-treatment (returned to treatment as usual), participants were maintaining gains on depression and suicidality
86
Q

IQ tests history

A
  • first developed by Simon and Binet to identify kids who might need help in school
  • because of eugenics, IQ testing was rooted in racist beliefs and used to identify people they thought shouldn’t be having children
  • IQ testing was based on cultural knowledge and test-taking skills so Black, Indigenous, poor people weren’t performing as well and institutionalized/sterilized
87
Q

cognitive abilities vs. intelligence

A
  • cognitive abilities: specific mental processes
  • intelligence: general quantity related to applying learned skills and knowledge in a variety of situations
88
Q

psychometric approach to intelligence

A
  • first standardized tests of intelligence
  • crystallized (acquired through schooling and experiences) and fluid (using your mind to solve novel problems, manipulating information)
  • crystallized increases throughout lifetime
  • fluid peaks in young adulthood, then declines as you keep aging
  • uses mental age (the level of age-graded problems that you can solve)
  • Stanford-Binet scales
  • Wechsler scales: WPPSI (preschool), WISC-V (6-18), WAIS-IV
  • score is based on how well you do relative to standardized norms for your age
89
Q

hierarchal view of intelligence

A
  • g: general intelligence (a latent value)
  • broad abilities (like fluid and crystallized) make up g
  • specific abilities assessed by specific tasks trying to tap into your broad abilities which allows us to hypothesize about your level of g
  • g = broad ability = score on tasks of specific abilities
90
Q

WISC-V

A
  • FSIQ made up of 5 domains
  • verbal comprehension: similarities & vocabulary
  • visual spatial: block design & visual puzzles
  • fluid reasoning: matrix reasoning & figure weights
  • working memory: digit span & picture span
  • processing speed: coding & symbol search
91
Q

IQ stability in childhood

A
  • starting around age 4, strong relationship with later IQ scores
  • but many children still show ups and downs throughout childhood (influenced by motivation, testing procedures)
  • IQ in infants is unrelated to later scores, EXCEPT for kids with moderate-severe ID
92
Q

IQ normal distribution

A
  • mean of 100, SD of 15
  • 95% of scores are within 2 SDs
  • 70 was IDD cutoff in DSM-IV (not in DSM-5)
  • 130 is giftedness cutoff
93
Q

racial ethnic intelligence disparities

A
  • not due to genetic differences between groups because race isn’t genetic
  • environmental differences: access to resources, adequate schooling, family income (low-SES; when you control for this, the gap shrinks)
  • stereotype threat
  • not only due to verbal tests: nonverbal items could also have cultural elements that interfere with one’s ability to do the task
94
Q

stereotype threat

A
  • things people know about stereotypes about their groups affects performance
  • stress about the stereotypes (confirming) interferes, can be unconscious
  • also because people tend to think of their intelligence as innate and fixed
95
Q

general ability index

A
  • similar to FSIQ but without processing speed (which itself is very reliant on working memory)
  • for people who still have the cognitive abilities to do the tasks, but work more slowly
96
Q

Gardner’s theory of multiple intelligences

A
  • 8 different dimensions of intelligence that don’t ‘add up’ to general intelligence like in the hierarchal view
  • linguistic, bodily-kinesthetic, inter/intrapersonal, visual-spatial, existential, naturalistic, musical, logical-mathematical
  • savant syndrome would be having very high intelligence in one type, and average in others
  • inspired ‘visual’ or ‘auditory’ learners
97
Q

Sternberg’s triarchic theory

A
  • practical (adapting, selecting, shaping environments), creative (dealing with novel problems, automatization), analytic (thinking critically, planning)
  • three components working effectively together = successful intelligence = adapt, achieve reasonable goals, optimize strengths and weaknesses
98
Q

Flynn effect

A
  • IQ estimate may be too high or too low depending when you take the test in relation to when it was normed (3pt increase per decade)
  • contributes to DSM-5 decision to remove IQ score cutoff (removing access to services)
99
Q

mild IDD severity

A
  • 85% of people with IDD
  • not identified until early elementary (we don’t see conceptual difficulties in preschool but language and social immaturity emerge in elementary)
  • kids from lower SES more likely to have mild IDD
  • as adults, will need support for complex independent tasks
100
Q

moderate IDD

A
  • 10% of kids with IDD
  • identified during preschool
  • more pronounced conceptual difficulties (expressive/receptive language, reading and writing)
  • modal level of severity in people with Down syndrome
  • as adults will function at elementary school level
101
Q

severe IDD

A
  • 3-4% of kids with IDD
  • clear organic cause
  • identified at young ages
  • limited speech (which affect social domain)
  • need lots of supervision and support for everyday activities
102
Q

profound IDD

A
  • 1-2% of people with IDD
  • identified in infancy
  • clear organic cause + co-occurring medical conditions
  • limited conceptual skills, language, nonverbal gestures
  • dependent on others for almost everything
  • still find pleasure in interaction
103
Q

IDD prevalence

A
  • 1-3%
  • more prevalent in lower SES (only for mild severity) and in males (again, only for mild)
  • as we increase in severity spectrum, organic causes spread evenly in all SES groups and genders
104
Q

IDD heritability and environment

A
  • heritability of intelligence is about 50% which means a large proportion can be worked on to enrich the environment and develop IQ
  • genetic influences are partially modifiable by the environment
  • phenotype can be affected by gene-environment interaction
  • heritability estimates decrease when SES is low (more environmental variability)
105
Q

organic causes of IDD

A
  • chromosome abnormalities, single gene conditions, neurobiological influences
  • tends to be moderate, severe, profound
  • comparable prevalence across SES
106
Q

cultural/familial causes of IDD

A
  • no clear cause
  • family history of IDD, economic deprivation, inadequate childcare, poor nutrition, parental psychopathology
  • tends to be mild
  • higher rates in low SES families
107
Q

chromosomal abnormalities

A
  • most common cause of severe IDD
  • Down syndrome (three copies of chromosome 21, most cases are random events)
  • Prader-Willi and Angelman (deletions of chromosome 15)
  • Fragile-X syndrome (part of the X chromosome is slightly bent, inherited)
108
Q

single-gene conditions

A
  • phenylketonuria (inherited, can be identified at birth and managed with restrictive diet to avoid IDD)
  • cannot metabolize phenylalanine so rising levels are toxic and can impact intellectual development
109
Q

neurobiological injury

A
  • prenatal (fetal alcohol syndrome)
  • perinatal (anoxia)
  • post natal (head injuries)
110
Q

Down syndrome comorbidity with IDD

A
  • 15-20% of people with IDD have Down
  • underlying symbolic abilities are intact (understanding abstract meanings)
  • delay in expressive language (more deficits than in receptive language)
111
Q

Down syndrome characteristics

A
  • fewer distress signals or desire for proximity with caregiver
  • delayed (but positive) self-recognition
  • delayed and abnormal internal state language
  • deficits in ToM = deficits in language and description of internal experiences
  • social skill deficits can lead to peer rejection (but still a desire for proximity)
112
Q

emotional and behavioural problems comorbidity IDD

A
  • rates much higher likely due to communication deficits, additional stressors, neurological deficits
  • impulse control disorders, anxiety and mood disorders most common
  • similar developmental patterns as typical children: internalizing problems more common in adolescence
  • ADHD symptoms are common, Pica (affects 8-10% across ages and levels of IDD), self-injurious behaviour
113
Q

physical and health disabilities comorbidity

A
  • higher prevalence of chronic health conditions
  • life expectancy for people with Down is about 60 yrs (cognitive decline after adolescence can contribute to this)
  • epilepsy, cerebral palsy common
114
Q

prevention of IDD

A
  • prenatal care (reduce neurobiological injury, increase gestation time, plan for uncomplicated delivery)
  • early care and education (safe and stimulating environments: remove lead paint, focus on speech and communication, preschool intervention, enrichment for low SES youth)
115
Q

disparities in early communication in high/low SES

A
  • parents with doctoral degrees speak to their children significantly more than parents who haven’t gone to university, and much more than parents on social assistance
  • leads to a projected word gap of 30 million in the first 3 yrs of life (differences in developing receptive language)
  • educational enrichment is especially important for low SES
116
Q

Carolina Abecederian project

A
  • low-income families with kids randomly assigned to receive a full-time educational intervention or be cared for at home
  • educational enrichment from infancy to preschool (5 yrs)
  • learning games, following the child’s lead and challenging them, focus on language
  • started seeing differences in IQ at 15 months, then dramatic differences at age 2-3
  • differences maintained when kids go to school (IQ, reading and math scores)
  • still see differences at 21 yrs, more people going to college
  • also see long-term benefits for the society (less crime, paying more taxes)
117
Q

behavioural approaches for IDD

A
  • initially a means to control/redirect negative behaviours
  • individuals have a right to a least restrictive effective treatment and one that results in safe and meaningful change
  • essentially reinforcement to teach skills and improve adaptive functioning
118
Q

CBT for IDD

A
  • self-instructional training and metacognitive training
  • verbal instructional techniques
  • teaching the child to be strategical (how to use strategies for effective living) and metastrategical (how to choose strategies for situations)
  • addressing a lack of generalization that is common (teaching something in one domain, but child finds it difficult to translate them to another situation)
119
Q

family-oriented strategies for IDD

A
  • helping cope with the demands of raising a child with IDD
  • some kids may benefit from out-of-home placement
  • generally, inclusion movement supports helping individuals integrate into society (regular classroom settings, teachers must adjust the curriculum)
120
Q

core features of autism

A
  • impairment in communication
  • impairment in social interaction
  • repetitive patterns of behaviour and interests
121
Q

impairment in communication ASD

A
  • about 50% of kids with ASD do not develop useful language
  • echolalia, perseverative speech, deficits in pragmatics (not taking into account context)
122
Q

impairment in social interaction

A
  • social imitation
  • joint attention
  • expressive nonverbal behaviour (communicating what you want, how you’re feeling - pointing)
  • reciprocity
  • social ‘mind’ (not thinking about people as possibilities for interaction, not interpreting the social nature of things or seeing the world as social)
  • theory of mind
123
Q

Theory of Mind

A
  • knowing that other people have mental states (desires, beliefs, intentions) that guide their behaviour
  • ASD have trouble taking others’ perspectives
  • assessed via False Belief tasks (Sally/Anne)
  • typical children reach this developmental milestone by age 4 (about 20% of kids with autism have reached it by then)
124
Q

repetitive patterns of behaviour and interests

A
  • self-stimulation (stereotyped, patterned, repetitive bx usually involving one or more senses)
  • intense, narrow interests (could be related to selective attention - filtering out social information in favour of these interests)
  • rigid routines (disruptions are even more upsetting that for typical kids)
  • preoccupation with parts of objects (only playing with the wheels of a car)
125
Q

self-stim theories

A
  • craving for stimulation that excites nervous system = reinforcement
  • blocking out/controlling unwanted stimulation from an overstimulating environment = calms down = reinforcement
126
Q

preoccupation with parts of objects

A
  • focus on parts of things when attending to social information (watching movies with eye tracking)
  • typical kids focus on faces to receive social information, kids with ASD don’t look at faces (only at parts of the faces or in the periphery
  • this avoidance of social information compounds over time = less social input = not developing skills to interact with your social world
127
Q

autism as categorical vs. dimensional

A
  • once viewed as a classic categorical disorder
  • now, it’s a spectrum: range of IQs, severity of symptoms, language abilities
  • family members tend to have autistic traits without meeting full criteria
128
Q

DSM-IV autism diagnoses

A
  • autistic disorder: social interaction + repetitive/restrictive interests + language deficits
  • asperger’s: social interaction + repetitive/restrictive interests
  • pervasive developmental delay, not otherwise specified (PDD-NOS): residual category
129
Q

changes in DSM-5 autism diagnosis

A
  • combining all previous diagnoses into one spectrum
  • criteria for DSM-IV were being applied differently across clinics
  • groups weren’t significantly different from each other - they all met criteria for the new ASD
130
Q

Autism Diagnostic Observation Schedule (ADOS)

A
  • semi-structured observation for assessment
  • tester engaging the person in tasks while rating their behaviour (like capacity for joint attention, reciprocity, etc.)
  • looking for unusual behaviours - the more are present, the more likely ASD is
  • has version for younger kids, teens, adults
131
Q

Autism Diagnostic Interview (ADI-R)

A
  • often paired with ADOS for assessment
  • interviews with parents/caregivers
  • trying to triangulate behaviour and get a more accurate diagnosis
132
Q

prevalence of autism

A
  • 1-1.5%
  • prevalence increasing over time (better identification and broader definitions?)
  • prevalent cross-culturally and at all income levels but large variation in diagnostic practices
  • 4:1 male to female ratio which increases to 10:1 for milder forms of autism
133
Q

course of autism

A
  • there could be symptoms before, but not reliably diagnosed before age 2-3
  • may be differences starting from birth
  • some lose developmental milestones that they previously achieved
  • usually lifelong (but variability in trajectories)
  • strong predictors of positive prognoses are better language skills and higher IQ (better social, academic, occupational achievement)
134
Q

efforts toward early identification

A
  • eye tracking to see what toddlers are looking at (with autism = focus on geometric figures rather than social images)
  • brain enlargement (cortical surface expansion between 6-12 months predicts autism diagnosis)
135
Q

ASD comorbidity

A
  • 70% also have IDD, 40% are severe-profound
  • 25% have splinter skills
  • 5% have isolated and remarkable talents (savant syndrome - difference in degree from splinter skills)
  • epilepsy
  • ADHD, conduct problems, anxiety, depression
136
Q

splinter skills

A

above average for the population and compared to yourself in other areas

137
Q

environmental etiological factors in ASD

A
  • toxin hypotheses: exposure of toxins as a causal factor
  • birth complications are a strong predictor (anoxia)
  • maternal factors like obesity, diabetes moderately associated
  • low in vitamin D, heavy metal exposure like mercury and lead (not necessarily causal, just an association)
138
Q

vaccine hypothesis of ASD

A
  • anecdotal evidence about kids starting to show autism symptoms around when they get their vaccines (esp. MMR)
  • worry about thimerosal and mercury
  • Wakefield: normal development + MMR = behavioural and GI problems (caused media outcry which increased rates of measles and mumps, but the paper was retracted and Wakefield fired)
  • later research not able to find any links between MMR/thimerosal/any vaccine and autism
139
Q

heritability of autism

A
  • 15-20% of siblings of people with autism also have autism
  • 70-90% concordance rates in Mz twins
  • 83% heritability estimate
140
Q

molecular genetics of autism

A
  • many possible areas on different chromosomes
  • complex genetic disorder
  • expression of ASD genes may depend on environmental factors during fetal brain development (epigenetics, etc.)
141
Q

etiology of ASD: brain development

A
  • not clear if causal
  • differences in structure (frontal lobe, cerebellum, medial temporal, limbic)
  • differences in function (decreased activation of mirror neurons especially in social situations, notshowing altered activation of facial recognition area when viewing mother vs. stranger)
  • structural and functional differences in the amygdala
142
Q

fad treatments for autism

A
  • vitamin supplements for B6, magnesium, etc,
  • gluten-free or secretin diets
  • secretin produced in the intestine, used to treat ulcers, but evidence shows it isn’t effective
  • anecdotal evidence for anything doesn’t mean it actually works
143
Q

psychotropic meds for ASD

A
  • used to treat co-occurring problems, not core features of autism
  • SSRIs for anxiety/OCD/depression
  • stimulants for ADHD
  • antipsychotics for aggression
  • work just as well as in typical kids, but be extra careful monitoring them in kids with ASD
144
Q

oxytocin for ASD

A
  • neuropeptide hormone involved in social bonding and social behaviours
  • studies showed improvements in social interactions for kids taking intranasal oxytocin (ToM, eye contact, social connection)
  • small samples so far, but promising
  • animal studies warn of potential long-term effects to be cautious of
145
Q

treatment strategies for ASD

A
  • decreasing disruptive behaviours
  • appropriate social behaviour
  • improving functional, spontaneous social communication
  • cognitive skills
  • adaptive skills to increase responsibility and independence
146
Q

Applied Behaviour Analysis (ABA) for ASD

A

(1) discrete trial training (structured behavioural approach) for behaviours that aren’t already present
- prompt the behaviour + reinforce the desired behaviour
- shaping: reinforce approximations/attempts of desired behaviour (every effort toward the behaviour)
(2) reinforce naturally occurring behaviour
- use of language, initiating conversation = reinforce = more likely to repeat that

147
Q

Developmental Social Pragmatic (DSP) models of treatment for ASD

A
  • targeting joint attention to improve social communication and interaction by being responsive to the child
  • promoting any type of communication (verbal or nonverbal) that the child initiates
  • pragmatic: just trying to communicate any way you can
  • building on what the child is doing
148
Q

two best established treatments for ASD

A
  • individual, comprehensive ABA
  • teacher-implemented, focused ABA + DSP
149
Q

individual comprehensive ABA for ASD

A
  • intensive (20-40hrs/week) for 2-3 years
  • start prior to 5 yrs
  • communication, social skills, behaviour management, pre-academic skills (teaching skills that will help you in school)
  • small studies show improvements in IQ and adaptive behaviour
  • gains could be achieved with 6-28 hrs/weeks
150
Q

teacher-implemented focused ABA + DSP

A
  • delivered in a classroom, less intensive than individual
  • reinforcing communication + ABA
  • associated with greater joint engagement in play activities with caregivers and teachers
151
Q

Yu et al. meta-analysis

A
  • broad: any ABA-type treatment (wide range of duration and dosage)
  • no impacts on receptive language, adaptive behaviour, daily living skills, IQ, restricted/repetitive bx, motor, cognition
  • saw good effects on socialization, communication, expressive language
  • not general improvements, but still positive
152
Q

Eckes et al. meta-analysis

A
  • only including comprehensive ABA (early childhood, 20-40hrs/week, personalized, promoting several skills at once, using multiple methods, one-on-one + group activities, requires parents)
  • good effects on intellectual functioning and adaptive behaviour
  • no improvements in language abilities, symptom severity, parental stress
  • language abilities may act as a moderator (greater receptive/expressive language at baseline = bigger intellectual gains)
153
Q

controversy around ABA

A
  • historical use of harsh punishment to reduce unwanted behaviours (like self-stim which isn’t harmful to anyone even if it is atypical)
  • dosage of intervention is way too intense
  • people with autism not being consulted about ABA implementation (is the intervention what is best for them, who advocates for kids and which behaviours should be reinforced or extinguished)
154
Q

Substance Use Disorder

A
  • problematic pattern of use leading to clinically significant impairment or distress as manifested by at least TWO symptoms in a 12-MONTH PERIOD
  • type of substance is a specifier
  • 4 main categories of symptoms: physical dependence (physiological), risky use, social problems, impaired control
155
Q

SUD symptoms (11)

A

(1) Substance is often taken in larger amounts or over a longer period than was intended.
(2) There is a persistent desire or unsuccessful effort to cut down or control substance use.
(3) A great deal of time is spent in activities necessary to obtain substance, use the substance, or recover from its effects.
(4) There is a craving or a strong desire or urge to use the substance.
(5) Recurrent substance use results in failure to fulfill major role obligations at work, school, or home.
(6) Continued substance use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the substance.
(7) Important social, occupational, or recreational activities are given up or reduced because of substance use.
(8) There is recurrent substance use in situations in which it is physically hazardous.
(9) Substance use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance.
(10) Tolerance, as defined by either or both of the following:
- A need for markedly increased amounts of substance to achieve intoxication or desired effect.
- Markedly diminished effect with continued use of the same amount of the substance.
(11) Withdrawal, as manifested by either of the following:
- The characteristic withdrawal syndrome for a substance.
- The same (or a closely related) substance is taken to relieve or avoid withdrawal symptoms.

156
Q

SUD specifiers

A
  • in early remission: None of the criteria have been met for at least 3 months but for less than 12 months (except “craving”)
  • in sustained remission: None of the criteria have been met at any time during a period of 12 months or longer (except “craving”)
  • In a controlled environment: where access to substance is restricted.
  • mild: 2-3 symptoms
  • moderate: 4-5 symptoms
  • severe: 6+ symptoms
157
Q

Separation Anxiety Disorder

A

(A) Developmentally inappropriate and excessive fear or anxiety concerning separation from those to whom the individual is attached, as evidenced by at least THREE symptoms
(B) fear, anxiety, or avoidance is persistent, lasting at least 4 WEEKS in children and adolescents and typically 6 MONTHS or more in adults
(C) clinically significant distress or impairment in social, academic, occupational, or other important areas of functioning.
(D) not caused by another disorder like ASD, delusions/hallucinations in psychotic disorders, agoraphobia, GAD, illness anxiety disorder

158
Q

symptoms in SAD (8)

A

(1) Recurrent excessive distress when anticipating or experiencing separation from home or from major attachment figures.
(2) Persistent or excessive worry about losing major attachment figures or about possible harm to them, such as illness, injury, disasters, or death.
(3) Persistent and excessive worry about experiencing an untoward event that causes separation from a major attachment figure.
(4) Persistent reluctance or refusal to go out, away from home, to school, to work, or elsewhere because of fear of separation.
(5) Persistent and excessive fear of or reluctance about being alone or without major attachment figures at home or in other settings.
(6) Persistent reluctance or refusal to sleep away from home or to go to sleep without being near a major attachment figure.
(7) Repeated nightmares involving the theme of separation.
(8) Repeated complaints of physical symptoms when separation from major attachment figures occurs or is anticipated

159
Q

Specific Phobia

A

(A) Marked fear or anxiety about a specific object or situation (in children, the fear or anxiety may be expressed by crying, tantrums, freezing, or clinging)
(B) The phobic object or situation almost always provokes immediate fear or anxiety.
(C) The phobic object or situation is actively avoided or endured with intense fear or anxiety.
(D) The fear or anxiety is out of proportion to the actual danger posed by the specific object or situation and to the sociocultural context.
(E) The fear, anxiety, or avoidance is persistent, typically lasting 6 MONTHS or more.
(F) clinically significant distress or impairment in social, occupational, or other important areas of functioning.
(G) The disturbance is not better accounted for by another mental disorder

160
Q

Specific Phobia specifiers

A
  • animal
  • natural environment
  • blood, injection, injury
  • situational
  • other
161
Q

Social Anxiety Disorder

A

(A) Marked fear or anxiety about one or more social situations in which the individual is exposed to possible scrutiny by others. Examples include social interactions, being observed, or performing in front of others (in children, the anxiety must occur in peer settings and not just during interactions with adults)
(B) The individual fears that he or she will act in a way or show anxiety symptoms that will be negatively evaluated
(C) The social situations almost always provoke fear or anxiety (in children, the fear or anxiety may be expressed by crying, tantrums, freezing, clinging, shrinking away, or failing to speak)
(D) The social situations are avoided or endured with intense fear or anxiety.
(E) The fear or anxiety is out of proportion to the actual danger posed by the social situation and to the sociocultural context.
(F) The fear, anxiety, or avoidance is persistent, typically lasting for 6 MONTHS or more.
(G) clinically significant distress or impairment in social, occupational, or other important areas of functioning.
(H) not attributable to the direct physiological effects of a substance or another medical condition.
(I) not better explained by the symptoms of another mental disorder
(J) If another medical condition is present, the fear, anxiety, or avoidance is clearly unrelated or is excessive
Specify: performance only

162
Q

Panic Disorder

A

(A) Recurrent unexpected panic attacks. A panic attack is an abrupt surge of intense fear or intense discomfort that reaches a peak within minutes and during which time at least FOUR SYMPTOMS occur (can emerge from either calm or anxious state)
(B) At least one of the attacks has been followed by 1 MONTH (or more) of one or both of the following:
(1) Persistent concern or worry about additional panic attacks or their consequences
(2) Significant maladaptive change in behavior related to the attacks
(C) Not due to a substance or other medical condition
(D) not better accounted for by another disorder

163
Q

Panic attack symptoms

A

(1) Palpitations, pounding heart, or accelerated heart rate.
(2) Sweating.
(3) Trembling or shaking.
(4) Sensations or shortness of breath or smothering.
(5) Feelings of choking.
(6) Chest pain or discomfort.
(7) Nausea or abdominal distress.
(8) Feeling dizzy, unsteady, light-headed, or faint.
(9) Chills or heat sensations.
(10) Paresthesias (numbness or tingling sensations).
(11) Derealization (feelings of unreality) or depersonalization (being detached from oneself).
(12) Fear of losing control or “going crazy.”
(13) Fear of dying.
Culture-specific symptoms should not count toward the four requires symptoms.

164
Q

Agoraphobia

A

(A) Marked fear or anxiety about TWO situations
(B) The individual fears or avoids these situations because of thoughts that escape might be difficult or help might not be available in the event of developing panic-like symptoms or other incapacitating or embarrassing symptoms
(C) The agoraphobic situations almost always provoke fear or anxiety.
(D) The agoraphobic situations are actively avoided, require the presence of a companion, or are endured with intense fear or anxiety.
(E) The fear or anxiety is out of proportion to the actual danger posed by the agoraphobic situations and to the sociocultural context.
(F) The fear, anxiety, or avoidance is persistent, typically lasting for 6 MONTHS or more.
(G) clinically significant distress or impairment in social, occupational, or other important areas of functioning.
(H) If another medical condition is present, the fear, anxiety, or avoidance is clearly excessive.
(I) not better explained by the symptoms of another mental disorder.
Note: Agoraphobia is diagnosed irrespective of the presence of panic disorder. If an individual’s presentation meets criteria for panic disorder and agoraphobia, both diagnoses should be assigned.

165
Q

situations in agoraphobia

A

(1) Using public transportation
(2) Being in open spaces (parking lots, marketplaces, bridges).
(3) Being in enclosed spaces (shops, theatres, cinemas).
(4) Standing in line or being in a crowd.
(5) Being outside of the home alone.

166
Q

Generalized Anxiety Disorder

A

(A) Excessive anxiety and worry (apprehensive expectation) occurring more days than not for at least 6 MONTHS, about a number of events or activities.
(B) difficult to control the worry.
(C) THREE (or more) of the following six symptoms (with at least some symptoms present for more days than not for the past 6 months).
Note: Only ONE item is required for children
(D) clinically significant distress or impairment in social, occupational, or other important areas of functioning.
(E) not due to the general physiological effects of a substance or a another medical condition
(F) The disturbance is not better explained by another mental disorder.

167
Q

GAD symptoms

A

(1) Restlessness or feeling keyed up or on edge.
(2) Being easily fatigued.
(3) Difficulty concentrating or mind going blank.
(4) Irritability.
(5) Muscle tension.
(6) Sleep disturbance (difficulty falling or staying asleep, or restless unsatisfying sleep).

168
Q

Obsessive-Compulsive Disorder

A

(A) Presence of obsessions, compulsions, or both:
(B) The obsessions or compulsions are time-consuming (e.g., take more than 1 HOUR PER DAY) or cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
(C) not attributable to the physiological effects of a substance or another medical condition.
(D) not better explained by the symptoms of another mental disorder

169
Q

Obsessions

A

(1) Recurrent and persistent thoughts, urges, or images that are experienced, at some time during the disturbance, as intrusive and unwanted, and that in most individuals cause marked anxiety or distress.
(2) The individual attempts to ignore or suppress such thoughts, urges, or images, or to neutralize them with some other thought or action (i.e., by performing a compulsion).

170
Q

Compulsions

A

(1) Repetitive behaviors (e.g., hand washing, ordering, checking) or mental acts (e.g., praying, counting, repeating words silently) that the individual feels driven to perform in response to an obsession or according to rules that must be applied rigidly.
(2) The behaviors or mental acts are aimed at preventing or reducing anxiety or distress, or preventing some dreaded event or situation; however, these behaviors or mental acts are not connected in a realistic way with what they are designed to neutralize or prevent, or are clearly excessive.
Note: Young children may not be able to articulate the aims of these behaviors or mental acts.

171
Q

OCD specifiers

A
  • with good or fair insight: recognizes that obsessive–compulsive disorder beliefs are definitely or probably not true or that they may or may not be true
  • with poor insight: thinks obsessive–compulsive disorder beliefs are probably true
  • absent insight or delusional beliefs: completely convinced that obsessive–compulsive disorder beliefs are true
  • tic-related: current or past history
172
Q

Major Depressive Disorder

A

(A) FIVE (or more) symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either
(1) depressed mood or irritability (only in youth) or
(2) loss of interest or pleasure
(B) clinically significant distress or impairment in social, occupational, or other important areas of functioning.
(C) not attributable to the physiological effects of a substance or to another medical condition
(D) not better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or other specified and unspecified schizophrenia spectrum and other psychotic disorders.
(E) There has never been a manic episode or hypomanic episode.

173
Q

MDD symptoms

A

(1) Depressed mood most of the day, nearly every day, as indicated by either subjective report or observation made by others. (Note: In children and adolescents, can be irritable mood.)
(2) Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by subjective account or observation).
(3) Significant weight loss when not dieting or weight gain or decrease or increase in appetite nearly every day. (Note: In children, consider failure to make expected weight gains.)
(4) Insomnia or hypersomnia nearly every day.
(5) Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down).
(6) Fatigue or loss of energy nearly every day.
(7) Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick).
(8) Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others)
(9) Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide

174
Q

MDD specifiers

A
  • anxious distress *also relevant for PDD
  • mixed features (manic)
  • melancholic (severe anhedonia)
  • atypical features *also relevant for PDD
  • psychotic features
  • catatonia
  • peripartum
  • seasonal
175
Q

Persistent Depressive Disorder

A

(A) Depressed or irritable mood for most of the day, on more days than not, as indicated by either subjective account or observation by others for at least two years (Note: only ONE YEAR in children in adolescents)
(B) Presence of at least TWO of the following:
- poor appetite or overeating
- insomnia or hypersomnia
- low energy or fatigue
- low self-esteem
- poor concentration or difficulty making decisions
- feelings of hopelessness
(C) During the 1 year period, the person has never been without symptoms for more than 2 MONTHS at a time

176
Q

PDD specifiers

A
  • anxious distress
  • atypical features
  • with intermittent major depressive episodes (1-2 distinct major episodes)
  • with persistent depressive episodes (meeting full criteria for MDD frequently or they last a long time)
177
Q

Disruptive Mood Dysregulation Disorder

A

(A) Severe recurrent temper outbursts manifested verbally and/or behaviourally that are grossly out of proportion in intensity or duration to the situation or provocation
(B) Outbursts are inconsistent with developmental level
(C) Outbursts occur, on average, 3 or more times per week
(D) Mood between outbursts is persistently irritable or angry most of the day, nearly every day, and is observable by others
(E) Symptoms are present for 12 MONTHS or more
(F) Not diagnosed before age 6 or after age 18
(G) Age of onset of outbursts are irritable mood is before age 10
(H) Child has never met criteria (except duration) for a manic or hypomanic episode (even lasting one day)

178
Q

Intellectual Developmental Disorder

A
  • includes both intellectual and adaptive functioning deficits in conceptual, social, and practical domains. The following three criteria must be met:
    (A) Deficits in intellectual functions, such as reasoning, problem-solving, planning, abstract thinking, judgment, academic learning, and learning from experience (clinical assessment and individualized, standardized intelligence testing)
    Note: no narrow IQ score cutoff, but the diagnosis wouldn’t be appropriate in people with IQs within 1SD of the mean
    (B) Deficits in adaptive functioning that result in failure to meet developmental and sociocultural standards for personal independence and social responsibility. Without ongoing support, the adaptive deficits limit functioning in one or more activities of daily life, such as communication, social participation, and independent living, across multiple environments, such as home, school, work, and community.
    (C) Onset of intellectual and adaptive deficits during the developmental period
179
Q

IDD severity specifiers

A
  • mild, moderate, severe, profound
  • not based on IQ scores, but impairment in domains of adaptive functioning
  • conceptual (ability to think), practical (performing adaptive activities), social (relationships) skills
180
Q

ASD criterion A

A

(A) Persistent deficits in social communication and social interaction across multiple contexts, as manifested by the following, currently or by history:
- Deficits in social–emotional reciprocity, ranging, for example, from abnormal social approach and failure of normal back-and-forth conversation; to reduced sharing of interests, emotions, or affect; to failure to initiate or respond to social interactions.
- Deficits in nonverbal communicative behaviors used for social interaction, ranging, for example, from poorly integrated verbal and nonverbal communication; to abnormalities in eye contact and body language or deficits in understanding and use of gestures; to a total lack of facial expressions and nonverbal communication.
- Deficits in developing, maintaining and understanding relationships, ranging, for example, from difficulties adjusting behavior to suit various social contexts; to difficulties in sharing imaginative play or in making friends; to absence of interest in peers.
*need all three

181
Q

ASD criterion B

A

(B) Restricted, repetitive patterns of behavior, interests, or activities, as manifested by at least TWO of the following, currently or by history:
- Stereotyped or repetitive motor movements, use of objects, or speech (e.g., simple motor stereotypies, lining up toys or flipping objects, echolalia, idiosyncratic phrases).
- Insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or nonverbal behavior (e.g., extreme distress at small changes, difficulties with transitions, rigid thinking patterns, greeting rituals, need to take same route or eat same food every day).
- Highly restricted, fixated interests that are abnormal in intensity or focus (e.g., strong attachment to or preoccupation with unusual objects, excessively circumscribed or perseverative interests).
- Hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of environment (e.g., apparent indifference to pain/temperature, adverse response to specific sounds or textures, excessive smelling or touching of objects, visual fascination with lights or movement).

182
Q

Autism Spectrum Disorder

A

(A) social communication + interaction (social-emotional reciprocity + nonverbal communication + relationships)
(B) TWO restrictive and repetitive interests and behaviours (motor movements, sameness/inflexibility, intense interests, hyper/hyposensory reactivity)
(C) Symptoms must be present in early developmental period (but may not become fully manifest until social demands exceed limited capacities, or may be masked by learned strategies in later life)
(D) clinically significant impairment in social, occupational, or other important areas of current functioning
(E) not better explained by IDD

183
Q

ASD DDx

A
  • Intellectual disability and autism spectrum disorder frequently co-occur; to make comorbid diagnoses of autism spectrum disorder and intellectual disability, social communication should be below that expected for general developmental level
  • Individuals who have marked deficits in social communication, but whose symptoms do not otherwise meet criteria for autism spectrum disorder, should be evaluated for social (pragmatic) communication disorder.
184
Q

ASD specifiers

A
  • With or without accompanying intellectual impairment
  • With or without accompanying language impairment
  • Associated with a known medical or genetic condition or environmental factor
  • Associated with another neurodevelopmental, mental, or behavioral disorder
  • With catatonia
185
Q

ASD severity specifiers

A
  • for A and B criteria, rate severity
    (1) requiring support
    (2) requiring substantial support
    (3) requiring very substantial support
186
Q

Social Communication Disorder

A
  • deficits in communication for social purposes
  • impairment of ability to change context for the needs of the listener
  • difficulties following rules for conversation and storytelling (taking turns, rephrasing when misunderstood, using verbal/nonverbal signals to regulate interaction)
  • restricted, repetitive patterns of bx and interests have never been present
187
Q

adolescents using mental health services from (1) most likely, to (10) least likely

A

(1) severe ADHD
(2) severe ODD
(3) nonsevere ADHD
(4) severe CD
(5) severe depression
(6) nonsevere depression
(7) nonsevere ODD
(8) severe anxiety
(9) nonsevere CD
(10) nonsevere anxiety