Personality disorder Flashcards
What is a personality disorder? DSM
A. An enduring pattern of inner experience and behaviour the deviates markedly from the expectations of the individual’s culture. This pattern is manifested in two (or more) of the following areas:
◦Cognition (i.e., ways of perceiving and interpreting self, other people and events)
◦Affectivity (i.e., the range, intensity, lability, and appropriateness of emotional response)
◦Interpersonal functioning
◦Impulse control
B. The enduring pattern is inflexible and pervasive across a broad range of personal and social situations.
C. The enduring pattern leads to clinically significant distress or impairment in social, occupational, or other important areas of functioning.
D. The pattern is stable and of long duration, and its onset can be traced back at least to adolescence or early adulthood.
E. The enduring pattern is not better accounted for as a manifestation or consequence of another mental disorder
.F. The enduring pattern is not due to the direct physiological effects of a substance (e.g., a drug abuse, medication) or a general medical condition (e.g., head trauma
What are the 3 ps?
Persistent – development by early adulthood at the latest
Pervasive – across a range of situations
Problematic –significant personal or interpersonal problems or distress
whats the 4th p?
Parsimonious – not accountable for by another psychological or psychiatric condition
Winsper et al 2019 epidemiology community prevalence?
Any PD - 7.8%
Cluster A - 3.8%
Cluster b - 2.8%
Cluster C - 5%
critique of the diagnostic approach
“A disappointing and confusing mixture of innovation and preservation of the status quo that is inconsistent, lacks coherence, is impractical, and, in places, is incompatible with empirical facts” (Livesley, 2010)
“Probably the most problematic is the revision of personality disorders, where they’ve made major changes; and the changes are not all supported by any empirical basis.” Chair of DSM-III Task Force Robert Spitze
How can a personality be ‘disordered’?
Socially deviant or statistically abnormal levels of a given trait
◦E.g. Extreme scores on Introversion
◦E.g. failure to develop certain components of personality e.g remorse
Developmentally “primitive” trait structure
◦Klein – a disordered personality is remains at the “paranoid-schizoid” level of development and does not achieve the “depressive position
Comorbidity - skodol 2005
Mean number of PD diagnoses = 1.4
◦Mean number of Axis 1 disorders = 3.4
Comorbidity - Clark 2007
Comorbidity rates of 50%◦Commonly comorbid with: mood disoders, substance misuse, eating disorders, social anxiety
Reliability - Skodol et al 1991
– with structured clinical interviews, median kappa for individual diagnoses = 0.77
BUT agreement between different structured interviews was .35-.50Stability is poor - beyond a few weeks, kappas fell to .36 -.4
Is PD persistent? (Zanarini et al 2007; Gunderson et al 2011)
PD is supposed to be persistent across the lifespan, yet 73.5% of a BPD sample remitted over 6 yearS
Can people with PD recover?
“symptoms” of BPD can remit. However, even after remission of BPD, problems in adaptive functioning are more stable than diagnose
DSM-V changes
Intended to move towards a dimensional model and retain the “clinical utility” of categorical diagnoses
Mixture model
◦Reduce the number of diagnostic categories to 6
◦Introduce dimensional assessment of relevant traits (e.g. empathy, identity, self-direction)
Critiqued for being “cobbled together” and “confusing”
Relegated to an Appendix for “research purpose
Strength of trait models in PD
Reliability is higher
◦Often high internal consistency e.g. .80-.93 for the DAPP, .71-.92 for the SNAP
◦Higher temporal stability - .82-.93 for the DAPP, .68-.91 for the SNAP
Weakness of trait model of PD?
Utility is lower
◦Who does and does not “have” a PD? Based on e.g. functioning, distress, etc.
◦Reliability lower (c. 0.27) if use cut-offs to develop quasi-diagnostic groups
adaptive failure - (Plutchik, 1980
unable to fulfil basic adaptive tasks: ◦Identity ◦Hierarchy (dominance/submissiveness) ◦Territoriality (belongingness) ◦Temporality (loss/separation
adaptive failure - livesley (1998)
– unable to achieve adaptive solutions to universal tasks
◦stable and integrated representations of self/others
◦intimacy and affiliation
◦prosocial behaviour and cooperation
how to improve our understanding of why people have “adaptive failure’?
we need to move away from a diagnostic, medical understanding of personality
Instead we need to look at the interaction of:
◦Biological factors (genes, neurology, temperament)
◦Learning history (trauma and attachment)
◦Cognitive factors (attention, memory, interpretation)
◦Interpersonal factors
(BioPsychoSocial model)
Genetic influences
% of personality variation due to genes
◦Coolidge et al (2001) - Heritability of DSM PD diagnoses ranged from .50 (paranoid) to .81 (dependent)
◦Heritabilities higher for dimensions (e.g. affective instability) than diagnoses (e.g. Torgerson, 1984; Zanarini et al, 2004)
Influence of “shared” environment is small. Specific experiences shape the other 50% of variation
Neurological influences
Increased sensitivity to affective information , e.g. increased activity in amygdala in BPD in response to negative pictures (Koenigsberg et al, 2009) and faces (Minzberg et al, 2007)
Decreased activity in areas of the brain which inhibit emotional reactions, e.g. in BPD amygdala activity correlates with dorsolateral prefrontal activity instead of orbitofrontal activity (New et al, 2007)
Gene-environment interactions
Genes affect environment - Inherited temperament affects parent-child relationship (Tellegen and Waller, 2013)
Genes interact with environment - Caspi et al (2002) –
Specific genetic marker associated with antisocial traits, but only with a history of childhood abuse
Genes moderate environment - Wager et al (2009)
– Patients with BPD and a history of trauma or abuse , but with a particular genetic polymorphism, had reduced levels of impulsive aggression
Dysfunctional beliefs
dysfunctional beliefs are found in all PDs
◦Patients with AvPD, DPD, OCPD, NPD, HPD, BPD and PPD display beliefs consistent with their specific disorder (Beck et al, 2001;
Arntz et al, 2004).
◦Only moderate path coefficients between personality disorders and specific beliefs.
“Borderline beliefs” and “schema domains” mediate between childhood abuse and borderline traits (Arntz et al, 1999)
attentional biases
bias to attend to belief-consistent, but results are inconsistent
Stroop disruption greater with PD-relevant than irrelevant negative words - Waller and Button (2002), Sieswerda et al (2006, 2007)
Attentional bias correlates with early experiences (sexual abuse) and reduces in “recovered” patients - Sieswerda et al (2007
Inrerpretation biases
Interpret experiences to “fit” with pre-existing beliefs◦BPD patients misinterpret neutral faces as negative (e.g. Dyck et al, 2009).Biases may be implicit and mood dependent:
◦Association between self-related stimuli and shame-related stimuli in BPD in the Implicit Association Test - Rusch et al (2007) ◦Anger induction in IAT increases self/anger association in ASPD and self/abuse association in BPD (Lobbestael et al, 2009)
Memory biases
people with personality disorders may show “better” memory for negative material than positive material
◦Patients with BPD may be impaired in “directed forgetting” of negative words (McClure, 2005; Domes et al, 2006)
◦Inconsistent whether this is an inability to forget (Domes et al, 2006) or enhanced remembering (McClure et al, 2005)
