337 BPD & ASPD Flashcards
1
Q
history of BPD
A
- origins in psychoanalytics
- Stern: hypersensitive, problems with reality testing, negative reactions in therapy (patients getting worse with Tx)
- patients not clearly neurotic or psychotic = on the ‘border’ (very broad name for someone not responding to Tx)
- Knight: pseudo-neurotic schizophrenia (both psychosis and neurosis)
- DSM-III: intense affect, impulsivity, relationship problems, brief psychotic experiences
- now stuck with the name despite it being not descriptive (“emotionally unstable disorder”)
2
Q
emotional instability
A
- emotions change rapidly and repeatedly (intense and unpredictable)
- difficult to control - angry outbursts common
- family members feel shifts to be unpredictable, don’t understand triggers
- people with BPD have increased amygdala activation for fearful and happy faces (below conscious awareness)
- giving more resources for emotional content = hypervigilance and hypersensitivity to emotional fluctuations
3
Q
neurochemistry of BPD
A
- low 5-HT (serotonin: mood regulation)
- treated with SSRIs = improvements in aggressive impulsivity (but not overall reduced symptoms, no effect on emotion instability)
- some evidence of DA dysfunction (antipsychotic meds effective as Tx, inferred through behaviours like impulsivity, sensation-seeking, emotion dysregulation)
4
Q
unstable relationships in BPD
A
- emotional instability often triggered by loss, rejection, disappointment (perceived/real)
- unstable representations of others (idealization to devaluation)
- fear of rejection + fear of becoming too attached = ‘testing’ others to get them to prove that they care
- don’t trust that others will stay
5
Q
spousal abuse in BPD
A
- men with BPD often high on BPD characteristics
- they have unreasonable standards, idealization/devaluation, blame partner when things go wrong, poor impulse control = violence
- could see the same pattern in women, but not studied
6
Q
unstable self-concept in BPD
A
- difficult to conceptualize a coherent self, often tends to be negative
- sense of ‘emptiness’ - feel as though they have no substance when alone and define themselves in relation to others
- value relationships highly: threat to relationship = threat to self
7
Q
unstable behaviour in BPD
A
- impulsive and self-damaging
- alcohol/substance abuse, spending sprees, risky sexual behaviours, gambling, eating binges
- NSSI conceptualized as unstable behaviour (suicide behaviours can also be conceptualized that way, though not impulsive)
8
Q
NSSI and suicide in BPD
A
- NSSI very common in BPD (partly because it’s a criterion)
- threat to relationship/loved one leaving is a common trigger for NSSI to regulate negative affect
- suicidal ideation very common, attempts as well (1 in 10 die by suicide)
- reasons for attempts: to escape, to punish self, revenge (rare), to make others better off (more common), assumption of manipulative intent but maybe just trying to communicate
9
Q
dissociation in BPD
A
- 75% experience paranoid ideas or episodes of dissociation
- more common and more intense in people with BPD, and triggered by lower required levels of stress
- endorse dissociation even more than people with PTSD
- dissociation understood as misperception, paranoid beliefs aren’t as firm as delusions
10
Q
BPD epidemiology
A
- prevalence = 1-2% (higher in clinical settings), more common in women
- runs in families, also find higher rates of externalizing, SUDs, MDD
- has a genetic component (twin studies)
- psychosocial stress factors are very important (early trauma, abuse, neglect have strong associations but nonspecific)
- wide heterogeneity in presentation (debate about what are the core features of the disorder, no criterion A)
11
Q
BPD comorbidity
A
- MDD 60%
- PTSD 35%
- BP 20%
- EDs 17%
12
Q
in BPD a distinct diagnosis?
A
- as a variant of depression: more chronic form (but evidence of distinct neural signatures)
- as a variant of PTSD (but you can have BPD without trauma, trauma not unique to BPD or PTSD)
13
Q
BPD course
A
- chronic
- evidence that a large majority can be treated
- more severe in younger populations
- suicidal and impulsive bx can improve with Tx, mood reactivity often persists but people learn how to cope
14
Q
dialectical behaviour therapy for BPD
A
- Marsha Linehan
- form of cognitive therapy, practice both acceptance and change
- need to accept the person for who they are AND try to change the way they live their lives to align with their values
- recognize emotions and their triggers
15
Q
biosocial theory of BPD
A
- biological predisposition toward big emotional responses, sensitivity to environment, problems regulating emotions
- paired with a chronically invalidating environment: parents minimizing, blaming, rejecting, attributing pejorative responses to kid’s emotions = even more difficulty regulating
- punished for your emotions = emotions become scary and threatening
- “i’m sad” “no you’re not” (met with erratic and out-of-touch responses) = teaching the kid that they’re wrong about their emotions or stop communicating emotions, emotions threatening
16
Q
psychodynamic theory of BPD
A
- innate aggression interferes with normal development, cannot integrate positive and negative perspectives of the self and others
- unresponsive family environment disrupts development of a stable sense of self + unable to self-soother because they can’t remember positive images of nurturing
17
Q
biological factors in BPD
A
- affective instability may be inherited
- serotonin linked with suicide and impulsivity
- dopamine linked with novelty seeking, reward pathways
- oxytocin interacting with family functioning (important in child-parent bonding)
- limbic and prefrontal abnormalities - uncinate fasciculus, OFC in emotion control, amygdala disconnection from PFC
18
Q
executive neurocognition
A
- being able to delay or terminate a given response (cognitive or motor) for the purpose of achieving another goal or reward that is less immediate
- cognitive/behavioural/motivational inhibition, interference control
19
Q
cognitive factors in BPD
A
- executive neurocognition deficits
- verbal/nonverbal memory deficits (autobiographical)
- social cognition: attending to negative cues, biases in emotion recognition, less likely to rate strangers as trustworthy
20
Q
EE in BPD and Tx
A
- criticism and hostility not linked to poorer outcomes
- people with BPD fare better in Tx with emotional overinvolvement (perhaps process it better because of fear of abandonment)
21
Q
pharmacological Tx for BPD
A
- antipsychotics and antidepressants, anticonvulsants, benzodiazepines, lithium
- modest benefits, not much research
22
Q
psychological Tx for BPD
A
- DBT
- mentalization-based therapy (psychodynamic)
- transference-focused psychotherapy (psychodynamic; correcting distortions in social perceptions)
- schema-focused therapy (cognitive, behavioural techniques to modify schemas)
23
Q
Cleckley psychopathy
A
- comprehensive early description including behavioural, affective, interpersonal features of psychopathy
- behavioural: impulsivity, antisocial behaviour, sexual deviancy, irresponsibility
- affective/interpersonal: egocentricity, superficial charm, lack of empathy
- behaviourally, a psychopath might not be coming into conflict with society but could be masking a severe affective/interpersonal deficit (psychologically-focused definition which explains why psychopathy isn’t equivalent to ASPD)
24
Q
DSM-III Antisocial PD
A
- strong emphasis on observable behavioural criteria (no affective/interpersonal traits) to improve diagnostic reliability
- tendency to violate the rights of others (deceitful, aggressive, antisocial behaviours)
- demonstrates the divide between antisocial PD (only behavioural) and psychopathy (which includes affective/interpersonal)
- roots of ASPD lie in psychopathy conceptualization
25
Q
Cleckley’s 16 criteria
A
- superficial charm and good intelligence
- no delusions or irrational thinking
- no nervousness or psychoneurotic manifestations
- unreliability
- untruthfulness or insincerity (lying without purpose just to see what happens)
- lack of remorse or shame
- inadequately motivated antisocial behaviour (impulsivity, whimsical and poorly thought out)
- poor judgment and failure to learn by experience
- pathologic egocentricity and incapacity for love
- general poverty in major affective reactions (but could mimic without feeling)
- specific loss of insight
- unresponsiveness in general interpersonal relations
- fantastic and uninviting behaviour with drink and sometimes without
- suicide rarely carried out
- sex life impersonal, trivial, and poorly integrated
- failure to follow any life plan
26
Q
psychopathy checklist
A
- Robert Hare, based on Cleckley’s criteria
- 20 items rated by interview and school/police records
- widely used for parole decisions, to predict recidivism
- emphasizes hostility and aggression, but not a lack of anxiety (which is still central)
- Hare emphasized that psychopaths can be successful, not necessarily criminal or violent
- average person scores about 4, score of 30+ indicates psychopathy
- factor analysis shows two factors (emotional-interpersonal and behavioural deviance)
27
Q
emotional-interpersonal factor in PCL
A
- charm, grandiosity
- lying, manipulation
- lack of remorse
- lack of emotional depth
- lack of empathy
- could be split into affective & interpersonal
28
Q
behavioural deviance factor PCL
A
- child behaviour problems
- juvenile delinquency
- boredom, impulsivity
- irresponsibility
- violent behaviour
29
Q
ASPD vs. psychopathy
A
- most inmates qualify for ASPD diagnosis, but less for psychopathy
- ASPD misses non-criminal psychopathy
- qualify for both ASPD and psychopathy = worst offenders
- individuals showing more affective/interpersonal features and fewer antisocial behaviours are rarely criminalized
30
Q
recidivism and psychopathy
A
- psychopathy is the best predictor of recidivism
- up to 4x more likely to re-offend (violently)
- still not a perfect predictor - is it good to be using PCL for parole decisions?
31
Q
ASPD prevalence
A
- 0.2-3% for males and females in the gen pop
- possible diagnostic bias explaining gender differences
- higher in criminal and hospital settings
32
Q
psychopathy prevalence
A
- difficult to measure in the population, but best guess around 1%
- over-represented in prison settings (esp. in max security)
- female inmate samples range 9-31%
33
Q
prenatal and birth etiological factors for ASPD/psychopathy
A
- low birth weight
- malnutrition (severe) during pregnancy
- lead poisoning
- mother’s use of substances/alcohol during pregnancy
- no direct causal link, but robust correlations (smoking during pregnancy and conduct problems)
- possible pathways: smoking could alter brain development, could affect NT systems, could affect birthweight which in turn affect conduct, moms who smoke could be somehow different in a way that predisposes to conduct problems
34
Q
genetic etiological factors
A
- familial aggregation
- twin studies suggest genetic contributions
- genes could = difficult temperament, impulsivity, tendency to seek reward, insensitivity to punishment (genes as a causal factor for antisocial bx in general, aggression, impulsivity)
- genes could moderate susceptibility to environmental risk factors (genes as a moderator)
- genes could increase likelihood for exposure to environmental risk factors like parental divorce or maltreatment (gene-environment correlation)
35
Q
gene-environment correlation vs. gene-environment interaction
A
correlation: likelihood of exposure to environments
interaction: susceptibility to environments
36
Q
MAOA gene
A
- MAOA degrade amine neurotransmitters (DA, NE, 5-HT)
- more MAOA = more degradation = lower levels of NTs (associated with depression)
- less MAOA = less degradation = higher levels of NTs (associated with impulsivity/aggression)
- could be main effects or interactions
37
Q
MAOA diathesis theory
A
- childhood maltreatment is a robust risk factor for conduct problems (but still most kids don’t go on to show criminal behaviours in adulthood)
- MAOA gene altering susceptibility to maltreatment (GxE interaction)
- no maltreatment = no effect of low or high MAOA
- severe maltreatment = high MAOA still more likely to engage in criminal behaviour, but low MAOA show very high levels of antisocial bx (very susceptible to maltreatment)
- suggests MAOA as a diathesis, but this would assume that genotype and environment are independent, which isn’t likely
38
Q
psychopathy and maltreatment
A
- retrospective and prospective evidence of more abuse in childhoods of people with higher PCL scores
- rGE (correlation, increase risk of exposure to environments): parents of kids with high PCL scores more likely to have high PCL scores (parents behaving erratically and aggressively and passed on genes)
39
Q
environmental etiological factors in ASPD/psychopathy
A
- maltreatment + GxE interaction (MAOA) and rGE (abuse and PCL scores)
- parents often lacking psychological and physical resources to cope with difficult children = inconsistent discipline (difficult to learn behavioural contingencies)
- seeking similar antisocial peers reinforces behaviour (active rGE)
- kids engaging in criminality and drug use at a young age (genetic predisposition) can change future opportunities and life path
40
Q
etiological GxE interactions
A
- biological parents with ASPD = more likely to develop antisocial traits
- biological parents with ASPD + adopted into families with adverse environments = even higher likelihood of developing antisocial traits
- genes moderating susceptibility to adverse environments
41
Q
societal influences on antisocial behaviour
A
- poverty and neighbourhood crime related to delinquency
- social selection hypothesis: psychopathology = drift down in society
- social causation hypothesis: poverty = psychopathology (Costello study showing causal association with parental supervision as the mediator)
42
Q
cultural factors in antisocial behaviour
A
- socialization of kids toward aggression leads them to become more aggressive (brought into a military environment when very young = they become aggressive adults)
- minority status associated with antisocial bx, likely driven by low SES
43
Q
treatment and distress ASPD
A
- without distress, little motivation to change = Tx is challenging
44
Q
SSRIs for ASPD/psychopathy
A
weak evidence that SSRIs reduce aggressive bx and increase interpersonal skills
45
Q
Tx effectiveness in ASPD and psychopathy
A
- some treatments can reduce rates of re-offending in criminal offenders
- but these treatments can also cause rates of re-offending to increase in psychopaths (emphasizing empathy and social skills = they get better at conning or manipulating)
46
Q
Liberia Tx and prevention study
A
- looking at poorly integrated ex-combatants (not psychopathy, but involved in drugs, crime, violence) who were conscripted very young and socialized to be violent
- looking at antisocial tendencies as acquired skills instead of personality traits
- randomly assigned to CBT only, cash only, CBT+cash, neither
- 8-week group cognitive therapy (self-control, emotion management, conscientiousness and perseverance, less impulsive), to shift self-image from outcast to society member
- cash only = no reduction in antisocial bx
- therapy = only short-term change in antisociality
- cash+therapy = persistent reduction in antisocial behaviour, values, self-control
- mechanism: therapy pushes you to see yourself as someone who could be better, cash allows you to implement the skills you learn in therapy (you can become that better person)
- found to be less costly (societal) than allowing crime to continue
47
Q
historical descriptions of psychopathy
A
- Kraeplin’s morbid personality
- Schneider’s affectionless personality
- Millon’s aggressive personality
- Pinel’s manie sans delire
- often synonymous with criminality, sociopathy, ASPD (but consistent desire to separate psychopathy from general criminality)
48
Q
triarchic model of psychopathy
A
- an alternative to the factors in PCL
- meanness, disinhibition, and boldness as the core of the syndrome
49
Q
dark triad of personality
A
Machiavellianism, narcissism, psychopathy
50
Q
Fowles’ model of psychopathy
A
- deficits in the Behavioural Inhibition System (BIS)
- hypoactive BIS and normal BAS = psychopathic symptoms
- poor punishment learning, weak behavioural inhibition
51
Q
primary psychopathy
A
- low levels of neuroticism
- hyporeaction BIS
52
Q
secondary psychopathy
A
- high trait anxiety/neuroticism
- hyperresponsive BAS but no deficits in BIS
53
Q
Lykken’s low-fear hypothesis of psychopathy
A
- fearlessness impedes normal socialization = psychopathic symptoms (no fear conditioning, reduced amygdala functioning)
54
Q
response modulation hypothesis
A
- abnormalities in selective attention = inability to consider contextual information that should modulate goal-directed behaviour
- once attention is directed to a goal, they can’t divert attention to context
