337 final Flashcards
1
Q
Wakefield’s Harmful Dysfunction
A
- harmful: value based on social norms
- dysfunction: failure of an organ system to perform according to its evolutionary design
- the cause of symptoms must be mental to be a ‘mental disorder’
2
Q
Skeptical view
A
- Thomas Szasz
- mental disorder is a label to justify medical intervention in a socially undesirable behaviour
- labels result in stigma and social control
- mental disorder should be an extension of physical and only be applicable to physical lesions
3
Q
Pure Value Concept view
A
- mental and physical disorders are judgments of desirability
- disorder is a deviation from an ideal state
4
Q
As Biological Disadvantage
A
- purely biological
- decreases survival and reproductive fitness
- must also include statistical deviance view
5
Q
Lillienfeld critique
A
- questions what is natural function (the primary function of an organ system) and what is a by-product
6
Q
Widiger proposal
A
- disorders are constructs that must be measured indirectly
- conceptualization will evolve as knowledge evolves
- multimodal: latent constructs are multiply determined and multiply expressed (a single etiology would be ideal, but is unlikely)
7
Q
five factors necessary for a valid classification system
A
- Clinical description: common clustered signs and symptoms
- Course: similar trajectory
- Treatment response
- Family history: should run in families
- Laboratory studies: biological and psychophysiological associations
8
Q
challenges of a categorical system
A
- Heterogeneity: people in one group should look similar to each other and different from people in a separate group (this isn’t always the case)
- Comorbidity: 50% of people with one disorder meet criteria for another; how do you know which problem to treat first? Will affect Tx, severity, and prognosis
9
Q
DSM-I and DSM-II
A
- 1952 and 1968
- few categories with no requirement for number of symptoms
- based on psychoanalytic definitions
- a first attempt to standardize
10
Q
DSM-III and DSM-III-TR
A
- 1980 and 1987
- based on a medical model
- empirical (not psychoanalytic, based on symptoms instead of etiology)
- based on a consensus of professionals to define inclusion/exclusion criteria and duration
- multi-axial classification
I: Major Clinical Disorders (the problem to treat)
II: Personality Disorders (not to treat, but could affect axis I)
III: Medical Conditions
IV: Psychosocial Stressors (context)
V: Global Assessment of Functioning (somewhat arbitrary)
11
Q
DSM-IV
A
- 1994 and 2000
- introduced distress and impairment as factors
- gave a definition of mental illness
- polythetic approach: certain signs and symptoms are neither necessary or sufficient
12
Q
DSM-5
A
- 2013
- removes multi-axial system
- some diagnoses get dimensional criteria
- new categories (OCD, PTSD is moved to Trauma)
13
Q
what could comorbidities be due to
A
- chance (partly)
- sampling bias (more severe clinical populations)
- diagnostic criteria (overlap between diagnoses)
- multiformity (comorbid disorders represent a third independent disorder)
- causal (one disorder is a risk factor for another)
- shared etiology causes multiple disorders
14
Q
which disorders are where in HiTOP
A
- SAD: internalizing - fear
- Agoraphobia: internalizing - fear
- Phobias: internalizing - fear
- Panic: internalizing - fear
- OCD: internalizing - fear
- MDD: internalizing - distress
- GAD: internalizing - distress
- PTSD: internalizing - distress
- Bipolar: internalizing - mania AND thought - mania (also closely related to psychosis)
15
Q
1-year prevalences of disorders from most common to least
A
- MDD
- SAD (specific phobias may be 2nd most common)
- PTSD
- GAD
- Panic
- PDD
- OCD
16
Q
lifetime prevalences of disorder categories from most to least common
A
- anxiety disorder
- mood disorder
- substance use disorders
- prevalence for any disorder is 46%
17
Q
vulnerability-stress correlations
A
- demonstrate that diatheses and stress aren’t independent
- stress generation: people who are more vulnerable may behave in ways that increase their stress
- scars: having had one illness may change your view of the world which can exacerbate your stress
18
Q
etiological heterogeneity
A
- there are many pathways to disorder
- captured by dimensional diathesis-stress models: low diathesis might still be capable of developing disorders at high enough levels of stress (not all-or-none like the original categorical diathesis-stress model)
19
Q
differentiation between syndrome, disorder, disease
A
- syndrome: cluster of signs and symptoms that tend to co-occur, but pathology and etiology aren’t well-understood
- disorder: syndromes that cannot be explained by other conditions
- disease: most understood - both pathology and etiology
20
Q
endophenotype approach vs. exophenotype approach
A
- endo: focus on identifying reliable biomarkers or lab indicators that are only present in the disordered population
- exo: focus on traditional signs and symptoms (DSM’s approach)
21
Q
follow-up design
A
- start with people who are already ill and follow-up over time (prospective)
- studying the natural course of a disorder
22
Q
high-risk design
A
- start with a sample likely to develop psychopathology and follow-up over time (prospective)
- temporal ordering
23
Q
vulnerability marker
A
- should be present before, during, and after the illness
- if only after, could be a scar
- if it resolves with the illness, could be a subthreshold presentation
- should be over-represented in high-risk populations
24
Q
case control design
A
compare group with disorder to group without disorder (useful for rare disorders)
25
Q
cohort design
A
single large sample, some of whom have the disorder (to compare to many control groups, useful when the disorder is common)
26
Q
family studies
A
- identify proband and assess their family members
- rates of illness should be higher than in the general population
- family tends to have subthreshold presentations (we inherit traits or predispositions, not disorders)
- coaggregation: disorders run in families in a nonspecific way (depression and anxiety coaggregate in familires)
- can suggest a genetic role but doesn’t prove it (move to adoption studies)
27
Q
adoption studies
A
- parent as proband: find the kids they gave up for adoption to see if they’re ill
- adoptee as proband: compare their adopted/biological families to disentangle environment/genetic contributions
- cross-fostering: kids of parents without a disorder raised in families of people with disorders compare to kids of parents with disorders raised in families of people without disorders
28
Q
twin studies
A
- gives an additive genetic component (A) that is roughly the difference between the Mz concordance and Dz concordance
- common environment: shared environment
- unique environment: nonshared environment
- heritability estimate is sample-specific and varies according to environment - tends to increase with age and is higher when there’s less environmental variance
29
Q
endophenotypes
A
- intermediate between genotype and phenotype
- must correlate with illness in the population
- must not be state-dependent
- must be heritable (more in Mz than Dz)
- must see family similarities
- must be more present in families than in the general population
- must be specific to a particular illness (ideally)
- able to be measured
30
Q
fear
A
response to a real/perceived threat (prep for action) that is current, response is immediate and not mediated by conscious thought)
31
Q
panic
A
physiologically similar to fear but evoked without an identifiable or current threat
32
Q
anxiety
A
future-oriented (feeling threatened by potential occurrences that have not yet happened)
33
Q
epidemiology of specific phobias
A
- 2F:1M
- tends to have childhood onsets, but kids usually outgrow them (except for agoraphobia which onsets in 30s)
- high comorbidity with other anxiety disorders and depression
- prevalence is 12.5% for specific and 1.5% for agoraphobia
34
Q
etiological models of specific phobias
A
- classical conditioning: averse learning experiences = acquired fears (doesn’t explain all cases)
- fears maintained through operant conditioning (avoidance is negatively reinforced and fear cannot be disconfirmed - two-factor model)
- evolutionary preparedness: evolved sensitivity to certain stimuli
- immunizing effect of prior experience (kids have very little experience with anything)
35
Q
Klein’s theory of panic
A
- physiological sensations becomes the CS that was paired with a full-blown panic attack (the CR)
- leads to reinforcement through avoidance
36
Q
epidemiology of panic disorder
A
- 2F:1M
- 4-5% lifetime prevalence
- onset is about 24 years and very abrupt (rare before adolescence and after middle age)
- heritability estimate about 30-40%
- very comorbid with other Axis I disorders (and personality disorders common too)
37
Q
Clark’s theory of panic
A
- catastrophic misinterpretation of bodily sensations = more arousal = vicious cycle (initial symptoms are usually internally-generated, but could be due to caffeine, cocaine, etc.)
38
Q
anxiety sensitivity
A
- trait-like fear about sensations related to anxiety
- belief that if you keep having the panic symptoms, your health will eventually decline
- more likely to panic when you experience anxiety
39
Q
behavioural signs of PD
A
- safety behaviours: maladaptive coping contributes to maintenance of PDP
- interoceptive avoidance: avoidance of internal symptoms that reproduce high arousal (caffeine, having sex, saunas)
- experiential avoidance: distraction from anxiety sx, thought suppression
40
Q
temperament relation to panic
A
- neuroticism, negative affectivity
- fear of fear could lead to behaviours that exacerbate stress
- related to anxiety sensitivity
41
Q
etiology ideas from reading about panic
A
- anxious attachment (unpredictable/unresponsive caregiver) = anxiety disorders
- respiratory disease is common (could be a diathesis)
- reduced amygdala volume
- increased HPA reactivity to environmental cues (difficulty differentiating between threat and safety cues)
42
Q
treatment for PD
A
- CBT: panic control treatment uses cognitive aspects, conditioning, behavioural exposure (Clark’s model is more focused on cognitions)
- ACT useful if you use behavioural exposure
- exposure + relaxation + breathing training
- SSRIs most useful, benzos also effective (both have withdrawal effects that could prompt relapse)
43
Q
epidemiology of GAD
A
- 2F:1M
- 5-6% (lifetime) or 3.1% (6-month)
- onset is around 30 years, but highly variable
- gradual onset
- very chronic (similar to personality disorders)
- high comorbidities (controversial diagnosis because of this - could just be conceptualized as negative affectivity that predisposes generally to psychopathology)
- trait anxiety runs in families, so does GAD
44
Q
differentiation of GAD from MDD
A
- GAD: attentional biases toward threat
- MDD: more likely to have memory biases
- MDD: low positive affect (people with GAD can experience joy, but both have tendencies toward high negative affect)
- intolerance of uncertainty is the core feature of GAD
- MDD: precipitating event is humiliation vs. GAD: precipitating event is danger events
- MDD: emotion context insensitivity (ECI) - disengagement from the environment in lab stressors
- GAD: hyperresponsivity to threat and normal responses to positive stimuli in lab stressors
45
Q
temporal course MDD and GAD
A
- extreme goal-focus in GAD = burnout = motivational disengagement in MDD
- uncertainty about future in GAD = certainty about negative future in MDD
- beliefs of helplessness in GAD = hopelessness in MDD
- Or MDD could be a stressor, so after recovery people worry to prevent another episode
46
Q
cognitive avoidance
A
- rather than feel fear, worry about what to do about fear
47
Q
Tom Borkovec GAD
A
- worry = cognitive avoidance about low-probability events
- when those events don’t occur, they believe their worry was effective, so they keep worrying to keep preventing the bad outcomes
- worry is a verbal/cognitive process that buffers form emotional arousal (no vivid imagery = cannot change fear structure)
- thought suppression = more intrusive worry = increases sense of lack of control = more worry
48
Q
intolerance of uncertainty in GAD
A
- core feature of GAD
- tendency to react negatively to ambiguous situations (preferring a negative outcome to an uncertain one)
- causal role in exacerbation of worry
- information-processing bias (more recall of ambiguous situations and more likely to interpret them negatively)
49
Q
metacognition view of GAD
A
- Type I worry: about daily events
- Type II worry: worry about worry
- belief that worry is a positive coping strategy, so they use it, but when they feel they can’t cope with a stressor = Type II worry = belief that worry is uncontrollable
50
Q
mood-as-input view of GAD
A
- implementing an ‘as many as you can’ strategy to response generation + negative mood = more perseveration (so the cycle continues)
51
Q
treatments for GAD
A
- CBT (most effective)
- relaxation training, psychoeducation, identifying triggers of worry, imaginal/in vivo exposure
- cognitive restructuring: targeting beliefs about worry, intolerance of uncertainty, negative problem-solving orientation, cognitive avoidance
- client preference for meds or behavioural Tx (CBT is better for long-term outcomes, but otherwise they’re similar)
- SSRIs, benzos, SNRIs, psychotropics to boost GABA, second-generation antipsychotics
52
Q
epidemiology of SAD
A
- 2F:1M (gender differences emerge in adolescence)
- 12% prevalence (2nd most common anxiety disorder, 3rd most common overall)
- high comorbidity with anxiety and depression (high self-criticism) - SAD may act as a risk factor
- lower prevalence in East Asian countries and among Hispanic and non-white populations (could be due to measurement problems)
- onset age around 16 (social re-orientation and importance of peer judgment in adolescence)
- moderately heritable
53
Q
Clark and Wells cognitive theory of SAD
A
- social situations activate negative beliefs about their social competency
- negative schemas interfere with their interpretation of the situation = see more danger and threat = more anxious = rejection is viewed as even more likely = more anxious
- internal self-focus during social interactions so they can’t focus on others’ judgments (which acts a safety/avoidance behaviour) and makes them less socially competent
- biased memory toward negative experiences which reinforces a negative self-schema
54
Q
post-event processing in SAD
A
biased rumination that confirms negative beliefs
55
Q
research paradigms SAD
A
- Stroop task: cannot disengage attention from social threat words
- dot-probe paradigm: attending preferentially to threat stimulus
- attentional biases could also be shifting away from threat (which can lead to missing positive cues from others)
56
Q
biases in SAD
A
- judgment: self-critical, overestimate the likelihood of negative outcomes
- memory: especially when info is personally relevant, negative intrusive memories of social situations
- imagery: in third person = negative view of the self = more anxiety (contributes to maintenance)
57
Q
risk factors in childhood for SAD
A
- parental anxiety
- insecure attachment = negative peer relations, interpersonal difficulties
- childhood maltreatment = negative, global, stable inferential style
- controlling/critical parenting
- accommodating parenting = behavioural inhibition is reinforced
58
Q
CBT for SAD
A
- cognitive restructuring
- in vivo exposure
- Clark and Wells cognitive therapy: shifting attention externally, decreasing safety and avoidance behaviours
59
Q
biological interventions for SAD
A
- SSRIs and SNRIs
- benzos (as-needed adjunct)
- MAOIs (last resort)
- atypical antipsychotics, anticonvulsants
60
Q
obsessions
A
- intrusive and inappropriate (ego-dystonic)
- recognized to be your own thoughts (not thought-insertion)
- contamination, uncertainty, aggressive, symmetry/exactness, sexual (less common in kids), somatic
- never act on obsessions, but still cause distress
61
Q
compulsions
A
- attempts to neutralize or suppress obsessions (to decrease anxiety)
- washing/cleaning, checking, repeating, mental (prayers, voluntary thoughts)
62
Q
epidemiology of OCD
A
- 1.5% lifetime prevalence
- slightly more common in males in childhood, but slightly more common in females in adulthood
- age of onset is about 19 years
- usually with gradual onset (often childhood onset)
- very chronic (full remission is rare)
63
Q
cognitive models of OCD
A
- while intrusive thoughts are very common, people with OCD consider them to be very upsetting + feel responsible and self-blame for any possible negative outcomes (which makes the thought more upsetting until they must perform the ritual to decrease anxiety)
- negative affectivity increases rates of intrusive thoughts
- deficits in STM: constantly re-checking because they can’t remember if they’ve already checked
- poor reality testing: difficulty distinguishing between real and imagined events (convinced that thoughts are true)
64
Q
intolerance of uncertainty in OCD
A
- believe they lack sufficient coping mechanisms or problem-solving skills to deal with threats
- compulsions are an attempt to increase certainty about outcomes
65
Q
moral TAF
A
belief that unwanted disturbing thoughts are just as bad as the actions themselves
66
Q
likelihood TAF
A
belief that having a thought will increase the chance that the outcome will occur (which makes disturbing thoughts even more upsetting)
67
Q
neutralizing obsessional thoughts study
A
- attempts to undo or prevent thoughts (checking, crossing out, lighting on fire)
- neutralizing immediately = decrease in anxiety and decrease in desire to neutralizing
- delayed neutralizing = desire to neutralize remains, but anxiety decreases naturally
- neutralizing isn’t just driven by anxiety, but by a sense of responsibility
68
Q
disgust proneness
A
- especially associated with contamination subtype, but also hoarding, ordering, other specific phobias
- runs in families, also has a learning component (vicarious)
- OCD more likely to believe there’s a danger of contamination (false alarm)
- difficult to extinguish the aversive conditioning, so can be difficult to treat
69
Q
cognitive-behavioural models of OCD
A
- maladaptive beliefs (inflated responsibility, need to control thoughts, intolerance of uncertainty)
- intrusive thoughts appraised as significant
- operant conditioning helps maintain the disorder
70
Q
treatment for OCD
A
- exposure and response prevention shows 50-70% improvement
- in vivo/imaginal exposure to provoke anxiety, but let anxiety subside naturally and don’t engage in rituals (helps to facilitate extinction)
- within-session habituation (anxiety decreases within one session) and between-session habituation (anxiety is initially lower with every session)
- inhibitory learning: new safety associations are being created
- SSRIs, tricyclics show 20-40% reductions (convenient but modest)
71
Q
epidemiology of PTSD
A
- 2F:1M (but rates of trauma are equivalent across genders)
- 7-8% prevalence (but rates of trauma are 50-60%)
- highest risk of PTSD is associated with assault and violence (but still PTSD only develops in 50% of people)
- rates vary culturally (may be due to time of measurement effects), predominant/distressing symptoms vary culturally
72
Q
predictors of PTSD
A
- gender
- familial psychopathology
- history of psychopathology
- internalizing sx in childhood (negative affectivity)
- childhood or previous traumas
- lower IQ
- nature of trauma (proximity, duration, risk to life, intention, psychological factors during the experience, *dissociation most important)
- level of social support following trauma (but PTSD tends to erode social networks)
73
Q
results of the co-twin PTSD study
A
- similar abnormalities in ExP+ and UxP+ that aren’t present in the other pair of twins which suggests the vulnerability factor hypothesis
- slight differences between ExP+ and UxP+ suggest the worsening course hypothesis
- symptom severity was correlated with hippocampal volume in the same person and in their co-twin
74
Q
hypotheses about hippocampal volumes in PTSD
A
(1) scar hypothesis: caused by trauma
(2) risk factor for trauma exposure (selecting dangerous environments)
(3) vulnerability factor for developing PTSD following a trauma (SUPPORTED, only found in ExP+ and UxP+)
(4) consequence of exposure to trauma (NOT SUPPORTED, if only in Exp+ and Exp-)
(5) manifestation/sign of PTSD (if only in Exp+)
(6) product of a sequel or complication of PTSD (worsening course - SUPPORTED, predicting one twin’s PTSD severity from the co-twin’s volume)
75
Q
dual-representation theory of PTSD
A
- autobiographical memories (verbally-accessible VAM): info consciously attended-to before, during, after trauma
- situationally-accessible memories (SAM): unconsious information not easily accessed
76
Q
social-cognitive theory of PTSD
A
- trauma can modify important beliefs about personal invulnerability, the world as a meaningful and predictable place, and the self as positive/worthy
- can affect agency, safety, trust, power/control, esteem, intimacy
- individuals will engage in (1) assimilation, alter interpretation of event, (2) accommodation, alter original belief slightly, or (3) overaccommodation, alter belief drastically
77
Q
conservation of resources theory
A
- traumatic stress occurs when most important resources are threatened (well-being, sense of trust)
78
Q
treatment of PTSD
A
- CBT is best, includes prolonged exposure (PE) to habituate to anxety and block negative reinforcement from avoidance
- cognitive processing therapy (CPT) targets unhelpful thoughts without a behavioural component
- stress-inoculation therapy (SIT) and present-centered therapy (PCT) focus on non-trauma
- biological: SSRI, SNRI, antiadrenergics, mood stabilizers, anticonvulsants (benzos aren’t effective)
- 40-80% remission with large drop out rates (avoidance)
79
Q
epidemiology of MDD vs. bipolar
A
- MDD: 2F: 1M
- bipolar: F=M
- MDD 10-20x more common than bipolar
- bipolar has earlier onset, more episodes, poorer outcomes
80
Q
Watson & Clark tripartite model
A
- to explain overlap between MDD and anxiety disorders
- depression-specific: anhedonia (few people with anxiety show this sx)
- anxiety-specific: physiological hyperarousal (may be better applied to panic/phobias)
- overlap: general distress/negative affectivity
- cannot explain all cases (SAD)
81
Q
epidemiology of depression
A
- 2F:1M
- MDD lifetime prevalence is 16-17%
- PDD lifetime prevalence is 3-6%
- rates tend to be lower in East Asian countries
- PDD rates are higher in industrialized countries
- presentation varies culturally: somatic complaints in Asian, Latin American, North African countries
82
Q
MDD course
A
- onset teens/mid-20s (can be preceded by low grade chronic depression)
- episodes last 5-6 months on average
- 20% of episodes are longer than 2 years
- 50% of people who have one episode will have at least another
- most people relapse (average of 5-6 episodes over lifetime)
83
Q
PDD course
A
- very chronic
- high likelihood of remission with relapse
- common to have PDD with intermittent episodes of MDD
84
Q
family studies of MDD and bipolar
A
- proband with MDD = family more likely to have MDD, not bipolar
- proband with bipolar = family more likely to have bipolar and MDD
- some disorders run more cleanly in families, there is some overlap
85
Q
McGuffin twin study design and conclusions
A
- Mz and Dz index twins with bipolar or MDD, then find their co-twins to see if they have mood disorders, MDD, or bipolar
- Bipolar appears more heritable (suggests 70% heritability)
- suggests 96% heritability of mood disorders in general (mood disorders have a genetic component)
- suggests 52% heritability of MDD
86
Q
Kendler twin study
A
- higher heritability estimates in female twins for depression which suggests more genetic factors in girls
87
Q
Parker’s parental bonding instrument
A
- Dimension 1: care, nurturance
- dimension 2: overprotection, control
- low care frequently reported, overprotection less so
- interaction between low care and high overprotection is especially important
88
Q
behavioural models of depression
A
- behavioural inhibition (cause) = receive less positive reinforcement from the environment = even less likely to engage in those behaviours (avoidance - negative reinforcement)
- interpersonal deficits can also decrease the amount of positive reifnrocement
- anhedonia = amotivation = avoidance because lack of energy and activities aren’t rewarding anyway
- cognitive factors: low self-esteem = high negative affect = high self-criticism = bad social performance (which confirms belief of low self-esteem)
89
Q
Beck’s cognitive triad
A
- negative views about self = negative views about the world = negative views about the future (these schemas act as a diathesis, filter information)
- schemas contribute to negative automatic thoughts containing cognitive distortions
90
Q
cognitive distortions
A
- all-or-nothing
- arbitrary inference (drawing negative conclusions without evidence)
- overgeneralization
- selective abstraction (not seeing the whole picture)
- magnification/minimization
- personalization (bad things happen because of you)
- emotional reasoning (something is true because of the strength of the emotion)
91
Q
Seligman’s learned helplessness
A
- learn early on that our behaviour is useless to change a situation, so we should stop expending effort to try (doesn’t explain why depressed people feel guilty for bad things happening)
- revision: we make internal, global, stable attributions when we feel like we lack control over a situation
92
Q
self-referent encoding task (SRET)
A
- lab study for memory biases seen in depression (preferential recall for negative words that they endorsed as describing them)
- we don’t see these memory biases in people with anxiety
- sometimes also seen in at-risk populations
93
Q
attentional biases in depression
A
- faster at finding threat in a safe environment and slower at finding safety cues in a threatening environment
- stroop task: difficulty disengaging from threatening or sad words
- dot-probe task
- dischotic listening: difficulty inhibiting distractor information when it’s related to loss, sadness, threat
- less evidence for attentional than more memory biases
94
Q
integrated view of depression
A
- diathesis can be biological (genetic, neurochemical (monoamines), endocrine (stress response), immunology (inflammation response), neural connectivity)
- can be behavioural (avoidance)
- can be cognitive (distortions, schemas)
- can be emotional (reactivity, regulation)
95
Q
treatment of depression
A
- behavioural: decreasing unpleasant and increasing pleasant events (behavioural activation)
- CBT: identify and challenge automatic thoughts, cognitive errors, negative core beliefs
- interpersonal therapy: identifying and correcting lapses in interpersonal functioning
- somatic: ECT, transcranial stimulation, deep brain stimulation, MAOIs, TCAs, SSRIs, SNRIs
- PDD especially can benefit from continued pharmacotherapy and psychotherapy
96
Q
psychotic symptoms in bipolar
A
- mood congruent (delusions of grandeur for mania, guilt and sin for depression)
- mood incongruent (thought insertion/mind control for mania, anything happy for depression)
- psychotics sx should only occur during the episode to still be considered bipolar, otherwise it’s schizoaffective
97
Q
epidemiology of bipolar
A
- lifetime prevalence is 2-4%, stable worldwide
- cyclothymia prevalence is 4-5%
- 5-10% with depression will convert to bipolar
- episodes last about 2 months (but duration can decrease with tx)
- poor prognosis if mixed states or rapid cycling
- relapse rate: 7-9 times over lifetime
98
Q
treatment for bipolar and MDD
A
- bipolar: lithium as mood stabilizer with anticonvulsants (has a lot of noncompliance)
- MDD: antidepressants (which can trigger mania in bipolar)
99
Q
goal-attainment etiological model
A
- stress in prior 6 months predictive of onset and relapse
- goal-attainment events can also trigger mania: get really happy = get dysregulated = no productive bx = downward spiral
- elevated reward sensitivity (NAcc activation, more reactive to successes - predictor of severe course)
100
Q
kindling etiological model
A
- need a high-level stressor to provoke the first episode = brain changes to be more vulnerable = need less stress for the next episode until no stress is required to provoke mania
101
Q
biological factors in bipolar
A
- high norepinephrine in mania, low in depressive
- decreased sensitivity of serotonin system = increase variability in dopamine system
- high glutamate levels in PFC
102
Q
neural circuits in bipolar
A
- hyperactive amygdala in mania
- decreased connectivity between amygdala and PFC
- lower PFC activation (inability to inhibit emotions, abnormal control of limbic structures)
- impairments in emotional control circuits
- hyperactive BG and striatal activation
103
Q
social rhythm stability hypothesis
A
- inability to maintain daily rhythms, increased variability in circadian rhythms
- fluctuations in sleep quality can trigger negative moods
- bright light can trigger mania (disrupting circadian rhythms)
104
Q
stressor
A
- external demand that presents a challenge to homeostasis/ability to maintain equilibrium
- can be negative or positive, real or perceived
105
Q
stress
A
- how the organism reacts physiologically/psychologically to the stressor
- necessarily and sufficiently an interaction between the organism and its environment
106
Q
SAM system
A
- sympathetic adrenomedullary system
- hypothalamus signals = medulla secretes adrenaline and noradrenaline = fight-or-flight = peripheral excitation
- immediate response
107
Q
HPA axis
A
- hypothalamus-pituitary-adrenal axis
- hypothalamus release corticotropin releasing hormone/factor = pituitary gland releases adrenocorticotropic hormone = adrenal cortex releases glucocorticoids = fight-or-flight (inhibit immune system)
108
Q
allostatic load
A
the amount of strain the stress system is under
109
Q
hippocampus
A
- memory, stress regulation
- strong reciprocal connections with the hypothalamus and many cortisol receptors
- acute stress decreases hippocampal activation
- chronic stress decreases hippocampal volumes (cell death, fewer connections)
- altered function of the hippocampus = cortisol hypersecretion (cannot dampen the cortisol response like it should)
110
Q
PFC
A
- slow to develop, so it’s easier to inflict damage on it (vulnerable to effects of stress)
- repeated stress = dendritic shortening
- severe child abuse = decreased PFC volume (cell death, reduced connections)
111
Q
5 patterns associated with ELS
A
- common
- increases risk of lifetime mental disorder
- nonspecific risk factor
- increases risk of psychopathology throughout life
- explains 30% of disorder onsets
- can disrupt brain development (maternal cortisol)
- can lead to persistent dysregulation of stress response systems
112
Q
fetal programming
A
- maternal stress passed to fetus via glucocorticoids (placenta), so infants develop hypersensitive stress response systems (increased baseline and reactive cortisol)
113
Q
factors that can buffer against stress
A
- men doing the TSST with their female partner (doesn’t work for women unless the male partner is making physical contact)
- pet ownership, doing the TSST with a dog
- physical exercise can protect against hippocampal degeneration, can improve mood immediately
- present-focused breath
114
Q
sleep deprivation effects on stress systems
A
- increases allostatic load (increases blood pressure, and night cortisol)
- can affect hippocampal volumes, alter mood and cognitive control
- bad sleep hygiene can decrease sleep quality and duration
115
Q
reactivity hypothesis
A
- larger heart rate responses and greater cortisol reactivity = future adverse health risks
- also hyporesponsiveness of cortisol associated with adverse outcomes
- stress-related circadian dysregulation (flatter diurnal cortisol slope)
116
Q
specificity models of ELS
A
- effects of ELS differ depending on type of stress
- doesn’t account for co-occurring ELS
117
Q
cumulative-risk models of ELS
A
- doesn’t account for type, severity, chronicity
118
Q
dimensional models
A
- experience-driven plasticity has specific influences on learning and neurodevelopment through synaptic pruning and myelination
- threat/harshness, deprivation, unpredictability
- measuring degrees of experiences in early life and making predictions about affective, cognitive, neural development that are similarly/differentially affected by these experiences
119
Q
suicide attempt
A
nonfatal self-directed potentially injurious behaviour with an intent to die
120
Q
suicidal ideation
A
- thinking about, considering, planning suicide
- can be defined very broadly or specifically, not always conceptualized the same way which makes it hard to study
121
Q
NSSI vs. suicide attempts
A
- both highly correlated, also with depression and suicidal ideation
- NSSI more prevalent and frequent, different methods, less severe, performs different functions
122
Q
NSSI functions
A
- to relieve negative emotions/regulate affect
- not with intent to die
- interpersonal: autonomy (sense of independence), interpersonal boundaries (who I am vs. others) or influence (trend), peer bonding, revenge (rarely endorsed), sensation seeking, toughness
- intrapersonal (frequently endorsed): affect regulation, anti-dissociation, anti-suicide, marking distress, self-punishment
123
Q
why is suicide difficult to study
A
- stigma
- low base-rate phenomenon
- cannot be studied retrospectively, so must be studied longitudinally which requires very large samples
- studying proxies for suicide because we can’t study suicide as an outcome which may not be representative
- ethically researchers must intervene if an attempt is imminent
- etiologically complex (difficult to get a good holistic picture)
- not much replication work
124
Q
epidemiology of suicidal behaviour
A
- high-income countries have higher rates of suicide
- men are 3x more likely to die from suicide (disparity even larger in high-income countries)
- women make more attempts than men, deaths by suicide are increasing for women
- sex and age patterns differ according to economic status of country and time
- death by suicide is more common in kids and younger adults
- sexual and gender minorities have higher rates
- white and First Nations have highest rates
- young children have much lower rates of suicide, except Black youth who have higher rates of death by suicide
125
Q
which disorders are more associated with suicidal behaviour in types of countried
A
- developed: PTSD, bipolar, MDD
- developing: PTSD, conduct, SUDs
126
Q
psychosocial predictors of suicidal ideation and attempts
A
- depression, hopelessness, impulsivity
- impulsivity hastens transition from through to action
127
Q
Edwin & Shneidman’s theory of suicide
A
- psychache (emotional pain) is the primary motivator (threshold has been surpassed)
128
Q
Roy Baumeister’s theory of suicide
A
- motivated by a need to reduce aversive self-awareness
129
Q
Thomas Joiner interpersonal theory of suicide
A
- perceived burdensomeness and low belongingness as motivators & hopelessness about both these things create desire for suicide
- capability to act on suicide desire requires overcoming fears of death and pain
130
Q
superordinate dimensions of suicide motivators
A
- internal self-oriented: hopelessness, psychache, need to escape, etc. (associated with greater intent to die and more preparation)
- communication other-oriented: desire to seek help, communicate, etc. (associated with lower suicidal intent because they represent a continued connection to people and desire to maintain connection)
131
Q
therapies and prevention for suicide
A
- dialectical behaviour therapy (for BPD)
- cognitive therapy for suicide prevention (CT-SP) based on Beck’s theory
- collaborative assessment and management of suicide risk (CAMS)
- prevention: reduce access to means, school-based interventions,
132
Q
ideation-to-action framework
A
- risk factors can predict ideation, but not attempts (difficult to study how one progresses from thought to action)
- Joiner’s interpersonal theory
- integrated motivational-volitional theory (O’Connor)
- mental disorders (depression), impulsivity, hopelessness are predictors of ideation
- specific disorders (PTSD), poor premeditation, access to lethal means are predictors of attempts
133
Q
integrated motivational-volitional theory of suicide (O’Connor)
A
- defeat and entrapment are predictors of suicide desire
- acquired capability, access to lethal means, planning, impulsivity explain the progression to action
134
Q
3-step theory of suicide
A
- first step: psychological pain (one’s existence is being punished with pain) and hopelessness about the future
- pain can be isolation, high burdensomeness and low belonging, defeat and entrapment, etc.
- second step: pain exceeds connectedness (to other people, a sense of purpose, an interest, etc.) and then ideation will escalate
- third step: ideation progresses to attempt through capacity (fear of death is difficult to overcome)
- capacity can be dispositional (lower pain sensitivity) or acquired (habituation to pain, injury, death), or practical (knowledge or and access to lethal means
135
Q
suicide
A
death resulting from intentional self-injurious behaviour, associated with an intent to die as a result of the behaviour
136
Q
interrupted attempt
A
takes steps toward making a suicide attempt but is stopped by another person prior to any injury or potential injury
