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”)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

BPD comorbidity

A
  • MDD 60%
  • PTSD 35%
  • BP 20%
  • EDs 17%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

pharmacological Tx for BPD

A
  • antipsychotics and antidepressants, anticonvulsants, benzodiazepines, lithium
  • modest benefits, not much research
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
  1. superficial charm and good intelligence
  2. no delusions or irrational thinking
  3. no nervousness or psychoneurotic manifestations
  4. unreliability
  5. untruthfulness or insincerity (lying without purpose just to see what happens)
  6. lack of remorse or shame
  7. inadequately motivated antisocial behaviour (impulsivity, whimsical and poorly thought out)
  8. poor judgment and failure to learn by experience
  9. pathologic egocentricity and incapacity for love
  10. general poverty in major affective reactions (but could mimic without feeling)
  11. specific loss of insight
  12. unresponsiveness in general interpersonal relations
  13. fantastic and uninviting behaviour with drink and sometimes without
  14. suicide rarely carried out
  15. sex life impersonal, trivial, and poorly integrated
  16. 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