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  1. about robins and guze, who added an extra criterion?
    • Waldman, lilienfeld, and hahey 1995
    • diagnosis should be able to predict response to treatment
    • although this has been considered an error in logic (cannot determine etiology from response to treatment--headache remedied by opiate agonist, although may not have been caused by a lack of opiates)
  2. open concepts
    • Meehl 77, 90
    • all dx are open concepts, fallible
    • fuzzy boundaries
    • unclear inner nature
    • list of indicators that are extendable, modifiable
  3. misconceptions about dx
    • mental illness is a mythi (szasz, 1960)
    • dx is pigeon holing
    • dx is unreliable
    • dx stigmatize--rosenhan 1973 study
  4. criticisms of the classification system
    • comorbidity: lilienfeld et al, 1994, pincus 2004
    • Drake et al 2007 says it is premature to assume comorbidity is actually overlap
    • Explanations for comorbidity: dx mutually influence each other, predispose to each other
    • clinical selection bias, seeking tx
    • proliferation of dx: means not improving science
    • neglect of attenuation paradox: improve reliability reduces validity (loevinger, 1957)
    • Evidence for a dimensional model: except schizo-spectrum disorders (Lenzenweger & Korfine, 1994)
    • AxisI and AxisII distinction: Harkness & Lilienfeld, 1997: no evidence of qualitative difference
  5. Dimensional approach to DSM
    • evidence of dimensionality of disorders, especially PDs
    • Widiger and Clark: 5 factor model Costa & McCrae, 1992
    • Accomodates for variations in normal and abnormal personality
    • Obstacles: FFM is not universally accepted
    • there are competing models that aree also well supported like Telegen's 30D model of personality AKA "Big 3" which is: positive emotionality, negative emotionality, and constraint.
    • Harkness and Lilienfeld argue that there is a difference between basic tendencies and character adaptations.
    • Basic tendencies: core traits
    • Character adaptations: b manifestations of traits
    • eg. some BT can be expressed (CA) in socially constructive or destructive ways, depends on moderating influences. The implication is that personality dimensions may not be sufficient to capture the full variance of personality disorders.
    • This is in response largely to heterogeneity: for example, not all schizotypes or even schizophrenics have same symptome profile or perform deviantly on all laboratory tasks--maybe we need to be OK with heterogeneity if we want to understand true psychopathology--there really may be different subtypes with various etiologies (Lenzenweger, 2010).
  6. When talking about switching to the dimensional system what is something that is good to talk about?
    • NID PCS: nomenclature, information retrieval, description, prediction, concept formation, sociopolitical (Blashfield and Livesly, 1999)
    • Then say: How will switching improve these things?
  7. eysenk 1965
    • conducted research on psychotherapy and made claims that it was useless
    • only reviewed 11 studies (eliminated hundreds of articles b/c were dissertations, theses, project studies, or not published in peer reviewed, file drawer phenomenon)
    • also eliminated studies without untreated controls
    • only if .05 significance did he count it
    • discounted if significant using subjective measures like TAT or rorschach
    • if sig differences were found using objective measures like GPA but not subjective, discounted study b/c outcome differences were inconsistent.
  8. effect size
    mean difference between two groups divided by standard deviations of control (Standardized mean difference)
  9. smith and glass 1977
    • compared psychotherapies to untreated groups
    • found no differences between different types of therapies although therapy was better than no therapy
  10. Studies to cite for 5httlpr
    • Risch et al. 2009: serotonin transporter linked polymorphic region
    • numerous prior association studies of the same polymorphism (without looking at envi risk factors) had not consistently shown strong or replicated association w/ depression
    • caspi et al 2003 finding of interaction sounded intuitive b/c of known association between stressful life events and depression (Brown et al. 1973) as well as the general efficacy of ssris on depression
    • Risch et al. looked at: interaction btwn genotype (ss, sl, ll) and number of stressful life events (0, 1, 2, >=3) and DSM IV or ICD-10 categorical description of depression or not.
    • total of 14 studies included
    • 14,250 participants
    • used logistic regression
    • 1769 had depression of total
    • genotype alone didn't predict depression
    • number of stressful life events did predict depression
    • no significant interaction
    • highlights difficulty in finding effects, especially meta analyses, and difficulty in interpreting replications because all divergent definitions and measures
    • must be careful because those who report significant effect might only find it for one genotype (SL) vs. the aggregate genotype originally reported by Casp . This is a big difference and one worth investigating since it doesn't necessarily consistute a replication.
    • MUNAFO et al. 2009 meta-analysis found no support for interaction either.
  11. definition personality disorder
    • oltsmann and emery (2007)
    • enduring pattern of inner eperience and behavior that deviates markedly from the expectations of the individual's culture.

    Notice cultural component. Is this different from axis I?
  12. characteristics of bpd
    • paris 1999
    • impulsivity
    • affective instability
    • cognitive symptoms
  13. prevalence bpd
    • paris 1999
    • 1-2% pop
    • says 75% women, but lenz 2007 say prob equal just women present for tx more
  14. comorbidity bpd
    • paris 1999
    • depression and ptsd
  15. course bpd
    • paris 1999
    • adolescence, peaks young adulthood, burns out by middle age
    • some criteria predict continuation of bpd from adolescence to adulthood, namely anger, suicidal threats, identity disturbances, emptiness
  16. biopsychosocialmodel/diathesis-stress model of bpd
    • Paris 1999
    • no biological markers specific to bpd
    • basid dimensions of BPD (impulsivity, affective instability, cognitive symptoms) show heritability
    • Siever & Davis 1991: neurotransmitter systems to personality traits and disorders
    • each of four systems (mood-affect, impulse-action, attention-cognition, anxiety) associated w/ biological and genetic markers
    • mood affect-norepinephrine overactive
    • impulse-action-serotonin associated w/ behavioral inhibition underactive
    • Linehan's emotional vulnerability: excessive sensitivity to invalidating envi and emotional stimuli, vicious cycle
  17. ethnicity
    shared social and cultural characteristics that have a bearing on psychological functioning (sue, 1991)
  18. vulnerability=
    • tends to be associated with more of a psychological perspective. A subset of risk factors that are endogenous to the individual that may serve as mechanisms in the development of the disorder.
    • Can be genetically or environmentally based.
    • Thought of as stable and enduring.
    • Juxtaposed with the notion of resilience.
    • Vulnerability model: essential to note that the emergence of psychopathology is the result of stressors overwhelming one's level of resilience.
    • Think of:
    • BPD: Linehan's biosocial model: client's emotional and behavioral dysregulation are elicited and reinforced by the transaction between an invalidating rearing environment and biological tendency toward emotional vulnerability.
    • OCD: Salkovskis 1996: exaggeration of risk, negative automatic thoughts, avoidant behavior, neutralizing behavior maintain obsessions. Person's appraisal of intrusions predictive of OCD. Excessive tendency for self-blame, overestimation of responsibility, intolerance for uncertainty, excessive morality. Then stress increases presence of intrusions to make perfect storm.
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