Exam content Flashcards

1
Q

classification of mental disorders

A

1) Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR) -> North America
2) International Classification of Mental and Behavioral Disorders (ICD-11, issued by WHO) -> international/Europe

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2
Q

diagnostic heterogenity

A

two cases that qualify for one disorder can have no shared symptoms, sometimes opposing

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3
Q

psychological abnormality

A

behaviour, speech, or thought that impairs the ability of a person to function in a way that is generally expected of them in the context where the unusual functioning occurs

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4
Q

psychopathology

A

scientific study of psychological abnormality and the problems faced by people who suffer from psychological disorders

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5
Q

psychological disorder

A

specific manifestation of psychological abnormality, as described by some set of criteria that have been established by a panel of experts

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6
Q

mental disorder

A

often used to convey the same meaning as psychopathology, but it implies a medical rather than psychological cause

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7
Q

how to define abnormality?

A

1) statistical rarity
2) personal distress
3) dysfunction
4) violations of social norms
5) diagnosis by an expert

*consider everything: usually some combination of criteria is needed to identify a person’s behaviour as abnormal

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8
Q

statistical rarity

A
  • assumes that abnormal psychological functioning occurs rarely
  • however there are some issues:
    1) rarity doesn’t always mean disordered
    2) some examples of unusual functioning are considered advantageous (ex. genius IQ)
    3) some extremely common conditions are missed
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9
Q

personal distress

A
  • common of many disorders, but not all (ex. manic episodes)
  • distress is also a normal part of life
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10
Q

personal (harmful) dysfunction

A
  • abnormal behaviour only disordered if symptoms prevent proper functioning in an area of life
  • does not consider effects on other people
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11
Q

violation of norms

A
  • violations of societal expectations of behaviours
  • some issues:
    1) criminals (not meeting diagnostic criteria for any disorder) violate norms
    2) social norms change over time and cultures (ex. homosexuality used to be part of DSM)
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12
Q

diagnosis by expert

A
  • abnormality is defined when diagnosticians apply criteria for disorders as specified in manuals
  • experts often disagree!
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13
Q

which experts can legally communicate diagnoses to the patient?

A

psychiatrists, clinical psychologists

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14
Q

psychiatrist vs psychologist?

A
  • psychiatrist: MD, specializes in medications
  • psychologist: graduate school, focus on therapy
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15
Q

other professionals in mental health field

A

psychiatric nurses, occupational therapists, counsellors, registered psychotherapists, psychiatric social workers

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16
Q

prehistoric concepts of abnormality

A
  • supernatural explanations for disorders, ex. evil spirits, demons
  • harsh treatments: trephination (skull drilling), magic, incantation
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17
Q

naturalistic explanations for psychological abnormality

A

ancient greek, persian and arabian world

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18
Q

ancient greek approaches to psychological abnormality

A

1) Hippocrates: considered biology; disturbances in bodily fluids (humours) caused disorders needed to be rebalanced ex. by blood letting; wandering uterus = hysteria
2) Plato: sociocultural influences on thought and behaviour (basis of not criminally responsible aka NCR)
3) Galen: first to suggest a form of psychotherapy; sympathetic listeners

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19
Q

Persian and Arabian World approaches to abnormality

A
  • Quran suggested compassionate attitudes
  • built asylums
  • Avicenna wrote one of the first medical texts that tried to describe mental disorders, emphasizing natural causes rather than supernatural
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20
Q

The Dark ages of approaches to abnormality

A
  • Europe in middle ages
  • extreme treatments: exorcisms, burning at stake, torture
  • milder: prayer, generally caring
  • usually administered by clergy
  • supernatural/spiritual view
  • eventually Greco-Roman thought rediscovered
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21
Q

beginnings of scientific approach to abnormality

A
  • pressure against supernatural accounts
  • consideration that physical and psychological disorders had common (biological) causes
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22
Q

development of asylums/workhouses

A
  • initial: cruel conditions (shackles, harsh treatments/punishments)
  • some tried to integrate with society (ex. farmwork)
  • reforms due to the Mental Hygiene Movement lead to compassion, clean and comfortable environment
  • however state not well-equipped, leading to overcrowding and regression to cruelty
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23
Q

Mental Hygiene Movement

A
  • Pinel and Rush
  • desire to protect and to provide humane treatment for individuals with mental illness
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24
Q

understanding abnormality through biology

A

1) heredity
2) beginning of classification
3) infection

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25
Q

early heredity theories

A
  • degeneration theory (Morel): deviations from normal functioning are transmitted by hereditary processes
  • phrenology (Lombroso): shape of the skull related to inheritance of criminality (pseudoscience, but bore idea of mental mapping)
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26
Q

beginning of classification (syndroms)

A
  • Kraepelin’s Clinical Psychiatry: attempted to classify mental illness, grouped symptoms into syndromes
  • also proposed that biological causes underpin mental disorders (somatogenesis)
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27
Q

infection as a cause of mental disorder

A
  • Krafft-Ebing suggested that general paresis of the insane (GPI) might be result of infection
  • now known to be syphilis
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28
Q

insulin shock therapy

A
  • inject enough insulin for coma/seizure
  • Sakel used to treat morphine addition withdrawal
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29
Q

electroconvulsive therapy (ECT)

A
  • introduced by Cerletti
  • used to treat schizophrenia
  • determined to only be beneficial for depressed patients
  • continues to be a modern treatment for depression (in safer ways, when asleep)
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30
Q

modern shock therapies

A
  • DBS: deep brain stimulation for depression
  • VNS: vagus nerve stimulation, activates PNS
  • rTMS: repetitive transcranial magnetic stimulation
  • MST: magnetic seizure therapy
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31
Q

lobotomies and LSD in Canada’s history

A
  • lobotomies performed despite little evidence for clear benefits
  • Cameron’s brainwashing and LSD studies had no informed consent or ethical review
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32
Q

beginnings of psychopharmacology

A
  • rejection of psychological perspectives, hard turn to pure biological explanations
  • chlorpromazine (know this!!) was a radical antipsychotic drug
  • lead to rapid deinstitutionalization of patients from hospitals
  • communities did not have resources to support -> beginning of intersection between homelessness and mental illness
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33
Q

theories of abnormal behaviour

A

psychodynamic, behavioral, cognitive, biological, cross-cultural, evolutionary, humanistic -> all work together in conjunction, some try to explain all of behaviour, some focus on particular classes or disorders

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34
Q

usefulness of a theory

A
  • needs to generate research and increase knowledge, does not necessarily need to be true
  • null hypothesis testing: theories are better when they can be disproved
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35
Q

single-factor theories

A

attempt to trace origins of particular disorder back to one factor

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36
Q

interactionist theories

A

behaviour is product of the interaction of a variety of factors

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37
Q

aims of theories about mental disorders

A

1) explain etiology
2) identify maintenance factors (not necessarily same as etiology, ex. in phobias)
3) predict the course of the disorder
4) design effective treatments

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38
Q

hypnotism and birth of psychoanalysis

A
  • Mesmer: hypnosis to realign disturbed magnetic fluid in body
  • Charcot: hypnotism
  • Breuer: cathartic method (talking freely under hypnosis)
  • Freud: psychoanalysis (root of therapy!)
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39
Q

psychodynamic perspective

A
  • psychosexual stages of development: fixation at a specific stage affects behaviour and personality
  • ‘insight’ in therapy is the cure
  • levels of consciousness: conscious, preconscious, unconscious (controls everything, inaccessible)
  • levels of personality: ego, superego, id
  • defense mechanisms: denial, displacement, sublimation, regression, repression (most fundamental according to Freud), projection, intellectualization
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40
Q

evaluation of psychodynamic perspective

A

limits
1) difficult to test empirically
2) biased measures, biased population (family members)
3) biased information collection: free association, childhood recollections, adult dreams
4) biased views implying superiority of men

contributions:
1) focus on early mother-infant relationship led to attachment theories
2) unconscious thoughts may be important in prejudice and stereotypes

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41
Q

behavioural theories

A
  • emphasize how new behaviours are acquired through gradual/continuous process of learning
  • people play passive role, learning directed by environment
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42
Q

traditional learning theory perspective

A
  • classical conditioning
  • still relevant in trauma, phobias, OCD, adjustment disorders
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43
Q

types of reinforcement or punishment in operant conditioning

A
  • positive reinforcement: adding something pleasant
  • negative reinforcement: removal of unpleasant stimulus
  • positive punishment: adding something unpleasant
  • negative punishment: removing something pleasant
  • intermittent better than continuous
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44
Q

what operant conditioning principle involves avoidance?

A

negative reinforcement

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45
Q

Mowrer’s two-factor theory

A

1) classical conditioning establishes aversive response
2) operant conditioning reinforces avoidance

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46
Q

social learning theory

A
  • importance of context and vicarious learning (via observation/inference)
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47
Q

Bobo doll experiment

A

1) adults interact with doll with either kindness or aggression
2) kids act similarly to the adult they observed

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48
Q

hallmarks of cognitive thoeries

A

1) thinking affects emotion and behaviour
2) thoughts can be monitored and changed
3) by altering one’s thoughts, a person will experience desired behavioural and emotional change

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49
Q

cognitive-behavioural model

A
  • thoughts, emotions, bodily sensations, behaviour
  • everything bidirectionally connected in response to environment
  • CBT: find and change negative loops
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50
Q

rational-emotive behaviour therapy (Ellis)

A
  • find maladaptive, rigid beliefs that influence behaviour and emotions
  • combat them through argument, criticism
  • this was unpleasant, and did not involve independent discovery
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51
Q

Beck’s cognitive theory

A
  • more independent experimentation compared to Ellis (socratic learning - questions)
  • proposed the cognitive triad:
    1) dysfunctional schemas: negative representations of ourselves and world, affects view of future
    2) information processing biases: negative skew towards information gathering (self-fulfilling prophecies) -> notice and adjust to modify schemas
    3) automatic thoughts: find and challenge
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52
Q

third wave approaces to CBT

A

1) theory and treatment based on mindfulness: acknowledge a role for cognition but not necessarily label as bad, emphasize role of attention in distress

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53
Q

humanistic and existential theories

A

1) Maslow: self-actualization
2) Rogers: person-centered

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54
Q

Maslow’s theories

A
  • hierarchy of needs
  • abnormality from failure to attain self-esteem for self-actualization
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55
Q

Rogers’ person-centered approach

A
  • saw personal experience as basis for improving the self- people can be their own therapists by listening to their own needs
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56
Q

biological models

A

1) genetics and behaviour: adoption studies and twin studies to separate effects of genetics and environment
2) neurotransmitters: too little or too much (production, receptors, deactivation, re-uptake) -> can sometimes be reductionist
3) PNS (specifically ANS): overactive SNS can be phobias, anxiety, while overactive PNS has protective effect
4) endocrine HPA axis: results in release of cortisol, sensitivity implicated in depression and anxiety (chronically active)

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57
Q

socio-cultural influences on behaviour

A
  • stigma
    1) public: typical societal response that people have to stigmatized attributes (discrimination, devaluation, negative attitudes)
    2) self-stigma: internalized psychological impact of public stigma
  • social support, ex in PTSD
  • gender stereotypes: ED in women
  • race and poverty: minorities and poor more often victims of discrimination/prejudice
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58
Q

anti-stigma campaigns in Canada

A

focus on social contact and support as a means of treatment (or at least first step)

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59
Q

integrative theories

A
  • all are systems theories: whole is more than sum of parts
    1) diathesis-stress perspective: predisposition to disorder interacts with experience to result in disorder (commonly used to explain schizophrenia)
    2) biopsychosocial model: environment, psychological response and biology all interact (DSM focus)
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60
Q

reasons to classify mental disorders

A

1) better understand and identify them
2) determine what treatments work for whom and what disorder, what are most effective
3) organize treatments
4) group people with similar features for research
5) heuristic based on symptom presentation
6) make predictions about disorder development
7) provide people with support/validation for their symptoms

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61
Q

the ideal diagonstic system

A

1) clusters of symptoms (predictable/meaningful)
2) etiology
3) prognosis
4) predict response to treatment
5) no overlap
6) perfect cure
*4-6: not true in real systems

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62
Q

assessment

A

information gathered systematically in the evaluation of a condition

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63
Q

diagnosis

A

determination or identification of disease/condition, statement of that finding

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64
Q

diagnostic system

A
  • system of rules for recognizing and grouping various types of abnormal behaviour
  • provides criteria for a disorder
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65
Q

characteristics of strong diagnostic systems

A
  • reliability: same outcome every time
  • inter-rater reliability: two or more people agree on someone’s diagnosis
  • validity (needs reliability): whether a diagnostic category describes what it is supposed to and whether it predicts accurately
  • concurrent validity: ability to estimate individual’s present standing on factors related to the disorder, but not part of it (ex. diagnosis correlation negative attentional biases in depression)
  • predictive validity: ability to predict future course of development
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66
Q

in/out/day-patient

A
  • in: staying in hospital, usually for monitoring or safety purposes
  • out: normal life, go to office for appointment
  • day: in-between, day in hospital, but don’t live there
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67
Q

history on classification of mental disorders

A

1) syndromes
2) WHO’s ICD
3) 1st DSM: very psychoanalytic
4) DSM-II: similar problems to first
5) DSM-II, 7th printing: homosexuality removed
6) DSM-III: some structure introduced
7) DSM-III-R: revised, removed controversial diagnoses
8) DSM-IV: disorders now required clinically significant status (dysfunction or distress)
9) DSM-IV-TR: minor revision
10) DSM-5
11) DSM-5-TR

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68
Q

DSM-III

A
  • multi-axis model: typical disorders, personality, medical, environment, subjective statement of functioning
  • atheoretical
  • operationally defined each disorder
  • polythetic orientation: people could be diagnosed without having met all criteria, just have to pass threshold
  • research used for first time
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69
Q

cons of diagnosis in general

A
  • stigmatization
  • loss of information (continuous spectrum reduced to labelled categories or binaries)
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70
Q

stigmatization example

A
  • Rosenhan study
    1) faked symptoms
    2) admitted to mental hospital with schizophrenia, treated with isolation, dehumanized –> so much stigma, nobody noticed they were healthy
    3) stop faking, released with schizophrenia in remission
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71
Q

DSM-5

A
  • eliminated axis system to avoid emphasis of one over the other
  • sections regrouped based on disorders that co-occur
  • personality disorders placed on main spectrum of clinical disorders, suggests that they are amenable to change and treatment
  • hoarding disorder seperated
  • some dimensional approaches (spectrum disorders)
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72
Q

issues in DSM diagnosis

A
  • categorical vs dimensional approach: might have people with subthreshold symptoms that are significantly impairing –> sometimes cannot get diagnosis to get treatment approved
  • comorbidity: more than one disorder in the same individual, some are really commonly grouped –> lines between are arbitrary
  • personality disorders: half are rare, also overlap with many primary disorders –> was supposed to have dimensional approach, but half abandoned (in appendix)
  • gender bias/sexism (ex. symptom descriptions have gender associations)
  • doesn’t consider stress, environment or protective factors
  • cultural bias, some diagnoses are culturally-bound
  • political criticism: diagnostic criteria important for health coverage
  • some panel members had financial ties to drug-industries
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73
Q

solutions to problems with current diagnostic systems?

A

1) promoting dimentional systems, ex. RDOC criteria: focuses on dimensions with subconstructs that underly many disorders
2) hierarchical taxonomy of psychopathology (HiTOP): subgroups of disorders based on relationship between symptoms

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74
Q

RDOC criteria groups

A

negative valence, positive valence, cognitive, social, arousal/regulation

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75
Q

research methods

A

experimental, quasi-experimental, correlational, case studies, single-subject, epidemiological, inheritance/genetic

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76
Q

experimental design

A
  • most empirical
  • ideally only one variable changed to test effect of changing IV on DV
  • random assignment
  • control group
  • null hypothesis: assumes no relationship between two variables
  • ethical implications: sham treatment/waitlist –> intentionally withholding treatment
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77
Q

placebo effect

A
  • people receiving sham treatment still get better
  • control: inert medication, control for time
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78
Q

normative comparison

A
  • compare to health controls that go through the same treatment procedure
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79
Q

controlling clinical-patient interactions

A
  • eliminate natural biases
  • single-blind: participant doesn’t know what condition they are in
  • double-blind: neither participant nor experimenter know conditions
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80
Q

internal validity

A

extent to which changes in DV were result of IV manipulation

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81
Q

external validity

A

generalizability of findings

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82
Q

confounds

A

additional variables that exert their influence at same time as IV, making it impossible to know which is causing the effect (low internal validity)

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83
Q

quasi-experimental

A
  • experimental group not randomly assigned, instead selected on the basis of certain characteristics
  • no manipulation of IV
  • everything else controlled
  • limits: can only make correlation conclusions, can be difficult to match participants on all factors except one that is the IV
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84
Q

non-experimental designs

A

1) correlational studies
2) longitudinal studies: correlational results over time
3) case-studies and single-subject: can’t generalize
*none can make causal conclusions

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85
Q

case study example

A

KC: anterograde/retrograde amnesia

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86
Q

ABAB case study

A
  • one person used as own control
  • remove and introduce a particular condition
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87
Q

epidemiological research

A
  • study of incidence/prevalence of disorders in a given population
  • incidence: number of new cases in a time period
  • prevalence: frequency of disorder at a particular point in time
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88
Q

inheritance/genetic studies

A

1) family: inferences about heritability –> if proband (starting person) and relative display same diagnosis or behaviour, they are concordant, higher concordance rates suggest more heritability
2) adoption studies
3) twin studies
*genetics never explains 100%, always some environmental effect, gene-environment interaction studies have intensified

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89
Q

epigenetics

A

study of how environment leads to changes in DNA and therefore gene expression

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90
Q

clinical significance

A

1) treatment’s practical utility
2) whether symptoms are sufficiently intense for distress or dysfunction

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91
Q

statistical significance

A

observed effect passes a threshold that suggests it was sufficiently unlikely to have occurred due to chance

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92
Q

limitations to assessments

A

only a sample of behaviour

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93
Q

what are good assessment tools dependent on?

A
  • ability to accurately detect some aspect of the person being tested
  • knowledge of how people in general fare on such a measure for comparison purposes (ex. norms)
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94
Q

test-retest reliability

A

same test generates same results for the same person

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95
Q

alternate-form reliability

A

two versions of the same test give correlated scores

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96
Q

internal consistency

A

degree of reliability WITHIN a test

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97
Q

split-half reliability

A

if one half is correlated to the other (ex. even responses and odd responses)

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98
Q

coefficient alpha

A

averaging intercorrelations of all items within a test

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99
Q

face validity

A

items on test resemble characteristics of concept being measured

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100
Q

content validity

A

test’s items are thorough and reflect all behaviours believed to be related to the overall construct

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101
Q

criterion validity

A

correlation between measure and tangible external criterion

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102
Q

construct validity

A

relation of measure to another measure of same concept within a specific theoretical framework (ex. self-esteem and self-efficacy)

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103
Q

clinical approach to prediction

A
  • clinical intuition is most important quality to draw on all info for an accurate assessment
  • better when dealing with patients case-by case
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104
Q

actuarial approach

A
  • more objective, unbiased and scientifically validated methods
  • more efficient for large datasets
  • do not generalize to practice setting
  • no prediction rules for most decisions
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105
Q

types of prediction

A

clinical, actuarial, machine learning/AI

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106
Q

types of assessment

A

biological (neuroimaging, more for etiology over diagnosis), neuropsychological, clinical assessment (interviews), intelligence, personality, behavioural/cognitive

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107
Q

biological assessment

A
  • rules out underlying biological conditions
  • brain imaging, neuropsychological testing (individual or multi-test batteries)
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108
Q

brain imaging techniques

A

EEG, CT/CAT, MEG, PET, MRI, fMRI, fNIRS

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109
Q

fNIRS

A

specific frequency of IR that passes through skull but not blood

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110
Q

EEG

A
  • measures changes in brain current
  • high temporal resolution
  • low spatial resolution
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111
Q

CT/CAT

A
  • x-ray images
  • high spatial resolution
  • small radiation doses
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112
Q

PET

A
  • radioactive ligands in blood
  • can study subcortical neurons, receptors, neurotransmitters
  • radiation
  • expensive
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113
Q

MEG

A
  • changes in brain current (with magnetic waves)
  • high temporal, high spatial resolution
  • expensive
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114
Q

MRI

A
  • images brain structure
  • high spatial resolution
  • expensive
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115
Q

fMRI

A
  • infer brain activity by blood flow and oxygen levels
  • high spatial resolution
  • medium temporal resolution
  • expensive
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116
Q

application of brain imaging

A
  • before and after changes of psychotherapy
  • how those with disorder differ from controls
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117
Q

neuropsychological assessment

A
  • objective determination of cognitive capacity, determines how current behaviour relates to brain functioning (normal or abnormal)
  • intelligence, memory, learning, executive function , visuospatial function, etc.
  • batteries: multiple tests, long and laborious but can pinpoint specific impairments
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118
Q

examples of neuropsychological assessment screening tools

A

1) bender visual-motor gestalt test: copy patterns and shapes
2) repeated battery for the assessment of NP status (RBANDS): 12 subtests that cover range of domains relevant to neurological impairment
3) montreal cognitive assessment (MoCA): brief, rapid tool for mild cognitive impairment
4) trail making test (connect numbers/letters in alternating way)
5) complex figure test: copy from memory
*need to compare these to norms

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119
Q

intelligence tests

A
  • IQ = mental/chronological age X 100
  • 15 = 1 std. deviation
  • Stanford-Binet Intelligence Scales
  • WAIS, WMS, WISC (children), WPPSI (preschool)
  • very good reliability and validity, stable construct over time
  • making block designs
  • Raven’s progressional matricies
  • arithmetic, similarities
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120
Q

clinical interviews

A
  • unstructured: open-ended questions, facilitates rapport, poor reliability (different questions asked by different interviewers), missing relevant details
  • semi-structured: questions guided by prompts and decision-trees, some flexibility to get details
  • structured: very specific questions and order, no connection, less efficient
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121
Q

personality assessment

A
  • projective tests: rorschach inkblot test, thematic apperception test (psychodynamic, validity questioned)
  • standardized tests: MMPI, MCMI
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122
Q

thematic apperception tests

A
  • patient interprets strange image
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123
Q

MMPI-2

A
  • minnesota multiphasic personality inventory
  • 567 true/false questions
  • assesses multiple aspects of personality
  • profile of scores on scales of personality characteristics built by comparing psychiatric and non-psychiatric groups
  • contrasted approach: items were chosen only if people known to have the characteristic the scale is intended to measure responded differently to the item than did people who did not have that characteristic
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124
Q

MCMI

A
  • millon clinical multiaxial inventory
  • helps clinicians with diagnostic judgements about personality disorders and other clinical syndromes
  • 195 true/false questions
  • 25 clinical scales, 5 validity scales
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125
Q

personality assessment inventory (PAI)

A
  • 4-point likert scale
  • 11 clinical, 4 validity, 5 treatment-consideration, 2 interpersonal scales
  • assess symptoms (mild to severe)
  • ex. OCEAN
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126
Q

norms

A

1) standard or pattern, expected behaviour
2) statistical representation of population, used as reference to identify what percentile an individual lies at

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127
Q

down sides of self-report

A
  • traits have overlap –> maybe there are no distinct parts to personality
  • people tend not to provide accurate reports
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128
Q

response sets

A

test testing attitudes that bias self report answers

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129
Q

acquiescent style

A

says yes to everything

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130
Q

socially-desirable responding

A

respond to make themselves look good, minimize the bad

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131
Q

demand characteristics

A

answer in a way they think the tester wants them to answer

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132
Q

behavioural assessments

A
  • observation
  • rating scales
  • reactivity: change in behaviour because they know they are being watched
  • observer drift: raters suffer from an idiosyncratic bias in their ratings over time
  • expensive, time-consuming
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133
Q

how do tests avoid dishonest answers?

A
  • sets of questions, where one has a question that everyone will answer a certain way to: ex. do you have strange beliefs about cars? if yes, do cars have their own religion?
  • detects malingering: amplifying mental health symptoms for a benefit
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134
Q

cognitive-behavioural assessments

A
  • questionnaires assessing your thoughts
  • self-monitoring: record own behaviours, thought, emotions
  • advancements with technology: real-time assessments
  • self-monitoring also fosters insight and awareness –> an intervention by itself
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135
Q

major depressive disorder prevalence

A

5-12.5%, 50% who have one episode will have another, ~90% of those who have two or three will have more

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136
Q

MDD episode length

A

average 6-9 months

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137
Q

MMD onset statistics

A
  • average age: early to mid-20s, now decreasing (ex. teens)
  • women at higher risk at all ages
  • comorbid with anxiety disorders (>50%) contributes to more severe and chronic depression
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138
Q

MDD DSM diagnostic criteria

A

1) 5 or more of the following symptoms, one of which is depressed mood or anhedonia (both subjective or observed)
- significant weight loss when not dieting or weight gain (+5%), or decrease in appetite
- insomnia or hypersomnia (+/- 2hr)
- psychomotor agitation or retardation (observable)
- fatigue or loss of energy
- feeling worthless or excessive/inappropriate guilt, which may be delusional
- difficulty concentrating or indecisiveness
- recurrent thoughts of death, suicidal ideation, attempt or plan
*symptoms must be most of the day or nearly every day for at least a two week period in the last month
2) distress or impairment (clinically significant)
3) not due to substance or medical condition
4) no psychotic disorder
5) never had manic/hypomanic episode

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139
Q

comments on MDD DSM criteria

A
  • removal of bereavement exclusion could lead to increased prevalence
  • number of criteria is contentious
  • some people will have full inter-episode recovery, others have lingering symptoms
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140
Q

anhedonia

A

markedly diminished interest or pleasure in all, or almost all activities (subjective or observation)

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141
Q

persistent depressive disorder aka

A

dysthymia (until DSM)

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142
Q

PDD prevalence

A

0.03

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143
Q

double depression

A

chronic low mood (PDD) + additional episodes of depression

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144
Q

examples of double depression

A

1) persistent major depressive episode (MDE): decrease in mood that stays consistent
2) intermittent MDE with current episode

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145
Q

examples of PDD

A

1) dysthymic syndrome: consistent low mood
2) intermittent MDE without current episode

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146
Q

PDD differences from MDD

A
  • more chronic
  • younger age of onset
  • higher comorbidity
  • strong family history
  • lower levels of social support
  • higher stress
  • more dysfunctional personality traits
  • less likely to respond to standard treatment, often needs combination
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147
Q

PDD theoretical concern

A

how differentiated is this from a normal-range of personality traits?

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148
Q

PDD DSM criteria

A

1) depressed mood most of the day, for more days than not for at least 2 years
2) presence, while depressed of two or more:
- poor appetite or over eating
- insomnia/hypersomnia
- low energy or fatigue
- low self-esteem
- poor concentration or indecisiveness
- feelings of hopeless ness
3) during the 2-year period (1 year for children/adolescents), person has never been without symptoms in (1) or (2) for more than 2 months at a time
4) criteria for MDD may be continuously present for 2 years
5) no manic or hypomanic episode, never met criteria for cyclothymia
6) not better explained by other mood disorders or substance/medication
7) significant distress/impairment

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149
Q

premenstrual dysphoric disorder (PMDD)

A
  • prevalence: 1.8-5.8%
  • acute depressive symptoms that accompany menstrual cycle
  • must occur in most cycles in the past year
  • research focuses on hormonal mechanisms (birth control, SSRIs can help)
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150
Q

other specified depressive disorder

A

1) recurrent brief depression (5+ symptoms, 2-13 days, each month for at least 1 year)
2) short-duration depressive episode (4-13 days, 5+ symptoms)
3) depressive episode with insufficient symptoms (at least two weeks)

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151
Q

unspecified depressive disorder

A
  • clinical impairment, but doesn’t meet specific criteria
  • “catch-all” label
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152
Q

mania

A
  • distinct period of elevated, expansive or irritable mood
  • lasts at least one week OR any duration if hospitalization necessary or interaction with law enforcement
  • increased energy, decreased need for sleep, racing thoughts, pressured speech, impaired attention/concentration/judgement
  • can lead to altercations, reckless activities, substance use, aggression
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153
Q

hypomania

A
  • less severe mania, only lasting at least 4 days
  • can be longer if did not cause significant difficulties to warrant mania
  • can sometimes be hard to distinguish between feeling “good”
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154
Q

mixed-state episodes

A
  • rare
  • depression and manic/hypomanic symptoms felt at the same time
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155
Q

bipolar 1 DSM criteria

A

1) manic episode
2) during manic episode, must have at least 3 symptoms (four if only irritable) present to a significant degree (noticeable change from usual):
- inflated self-esteem or grandiosity
- decreased need for sleep
- more talkative or pressure to keep talking
- flight of ideas or feeling of racing thoughts
- distractibility
- increase in goal-directed activity or psychomotor agitation (non-goal-directed)
- excessive involvement in risky activities
3) impairment in functioning, need of hospitalization or psychotic features
*no need for distress!
4) not attributable to substance/medical condition

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156
Q

bipolar 1 and MDD

A
  • depressive history not necessary for bipolar diagnosis
  • but most patients will have had MDD in the past or future
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157
Q

bipolar 1 prevalence and onset

A
  • prevalence: 0.8%, equal male/female
  • mean onset ~20, 50% show symptoms as teens
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158
Q

bipolar 2 DSM criteria

A

1) hypomanic episode
2) same symptoms as bipolar 1
3) episode associated with unequivocal change in functioning that is uncharacteristic of the individual when not symptomatic
4) disturbance in mood and change in function is observable to others
5) not severe enough for impairment or hospitalization, no psychotic features
6) not attributable to substance or medication
7) one or more depressive episodes

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159
Q

bipolar II prevalence

A

0.5%, equal in males/females

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160
Q

progression of bipolar disorders

A
  • manic symptoms often enjoyable and pleasurable at first
  • tend to progress into distress/impairment, where others are effected, risks have consequences, depressive episodes become more severe
  • hypomania/mania tends to last two weeks to four months
  • depressive episodes tend to last 6-9 months
  • suicide rates 10-15%
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161
Q

cyclothymia

A
  • chronic, less severe form of bipolar
  • hypomanic and depressive symptoms, but never reaches full DSM criteria for either (faster cycling)
  • at risk for developing bipolar disorders
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162
Q

cyclothymia prevalence and diagnosis

A
  • 0.4-1%, equal across genders
  • hard to get diagnosis: how to tell difference between normal fluctuation or disordered?
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163
Q

rapid-cycling specifier

A
  • four or more manic and or depressive episodes within a year
  • episodes separated by at least two months of full or partial remission, or by switch to opposite mood state
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164
Q

seasonal affective disorder (SAD)

A
  • recurrent depressive episodes tied to changing seasons, usually winter months with less daylight
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165
Q

SAD prevalence

A
  • general: 0.6-3%, 2-3% in Canada
  • approximately 11% with MDD have SAD
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166
Q

SAD etiology

A
  • focus on melatonin produced at night by pineal gland
  • but, medications that suppress melatonin are not very effective
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167
Q

peri-partum and post-partum onset depression prevalence

A
  • 10-15% of mothers with mood swings that do not resolve or are severe enough for MDD or manic episodes
  • 0.1% have post-partum psychosis, may lead to suicide (5%) or infanticide (4%, command hallucinations)
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168
Q

peri/post partum onset depression risk factors

A
  • family history of depression
  • previous personal depression
  • poor marital relationship
  • low social support
  • stressful life events concurrent/following childbirth
  • could adversely affect child
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169
Q

biological: genetic etiology of mood disorders

A
  • genetics
  • twin studies: high heritability of MDD (36%), huge heritability of BP (75%)
  • serotonin transporter gene (HTT): controls individuals reactivity to stress, short (s) allele associated with negative cognitive style and personality (higher rates of MDD in response to stress)
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170
Q

heritability

A

percent of variability that can be explained by genetics

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171
Q

psychological: personality etiology of mood disorders

A

1) dependency: relying on interpersonal relationships for identity; neediness, fearing abandonment, feeling helpless in relationships
2) self-criticism: particularly towards achievement, fearing failure, self-blame, inferiority, guild

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172
Q

psychological: behavioural models in etiology of mood disorders

A

1) Lewinsohn’s behavioural model: operant conditioning –> low rate of positive reinforcement via social and other rewards leads to extinction of those behaviours
2) Seligman’s learned helplessness model: remain in unpleasant situations because they start to believe they have no control, even when escape/control options exist

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173
Q

cognitive etiology of mood disorders

A

1) Ellis: irrational and distorted thoughts
2) Beck: negative bias in appraising stimuli from the environment –> cognitive distortions framework –> diathesis stress model: only after stressful event might schema start to cause difficulties

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174
Q

cognitive distortions

A
  • automatic thoughts because of underlying schemata about the self, world or future (negative)
  • awareness gives opportunity to notice and challenge them
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175
Q

appraisal theory

A

1) primary: challenge (potential for gain/growth) or threat?
2) if threat, secondary appraisal: effective options (low threat) or ineffective/no options (high threat)?

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176
Q

examples of cognitive distortions

A

1) all or nothing thinking
2) over generalizing
3) mental filter (attentional bias)
4) disqualifying positive
5) jumping to conclusions: mind-reading, fortune telling
6) magnification (catastrophizing) or minimization
7) emotional reasoning: assuming that because we feel a certain way, what we think must be true
8) should, must, ought (guilt with self, frustration with others)
9) labelling (self or others)
10) personalization (assuming responsibility for things that aren’t your fault or blaming others for things that were your fault)

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177
Q

attentional/interpersonal etiology of mood disorders

A

1) attentional bias
- depressed people preferentially attend to negative info
- more likely to be judged as less socially skilled because not as animated, more negative affect, angry/depressed feelings
- manic people preferentially attend to positive stimuli
2) depressed people tend to seek confirmation of criticism and other negative interpersonal beliefs from others, can provoke further negative responses
3) interpersonal dependency or excessive reassurance seeking: learn to need assurance, may compound social aspect because of annoyance

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178
Q

life stress perspective of mood disorders

A
  • depressed people 3x as likely to experience stressful life prior to onset
  • sudden losses or sudden changes
  • nearly 75% MDD suffered major loss event 3-6 months before
  • life events related to reward/goal attainment predict increases in manic symptoms
  • early child maltreatment: negative core schemas (Beck beliefs), taxes biological systems (HPA axis, cortisol)
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179
Q

biological: neurotransmitter etiology of MDD

A
  • deficiency in serotonin
  • SSRIs thought to raise serotonin in brain, but this may not be why they are valuable as antidepressants
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180
Q

biological: cascade hypothesis of depression

A

1) cortisol release during stress stimulates receptors in hippocampus
2) hippocampus inhibits HPA axis by negative feedback
3) chronic stressors result in sustained release of cortisol, breakdown of negative feedback (hippocampal degradation)

supporting studies
- HPA axis more reactive in females (2x depression)
- greater lifetime stress experience, smaller hippocampus
- child abuse associated with cell death in hippocampus and amygdala

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181
Q

sleep neurophysiology and mood disorders

A
  • loss of slow-wave (deep) sleep and earlier on set of REM stages in MDD
  • sleep deprivation can induce symptoms of mania, people suggest that BP is related to sleep dysregulation
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182
Q

neuroimaging mood disorders

A
  • depression associated with decreased blood flow and reduced glucose metabolism in prefrontal cortex (reversed in mania)
  • increased glucose metabolism in subgenual anterior cingulate cortex (ACC), seems to be related to attentional biases
  • increased activity in amygdala, maybe also related to attentional biases
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183
Q

CBT for depression

A
  • goals: increase awareness of thoughts and appraisals to events, examine their contribution to emotions
  • structured format, 16-20 sessions
  • socratic questioning, guided collaborative discovery
  • activity monitoring and scheduling (behavioural activation): to counteract Lewinsohn’s theory, this is a critical component!
  • thought records to challenge distorted thinking
  • behavioural experiments
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184
Q

CBT success with depression

A
  • some evidence of being superior to psychodynamic psychotherapy
  • comparable results to antidepressants and IPT
  • lower relapse rates in the long-term
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185
Q

mindfulness based cognitive therapy (MBCT)

A
  • Buddhism principles
  • promotes non-evaluative awareness of present
  • detach from ruminative thinking, cultivate detached perspective
  • helpful for avoiding relapse
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186
Q

interpersonal psychotherapy (IPT) for depression

A
  • based on psychodynamic theories viewing loss and disordered attachment as underlying factors
  • assumes depression occurs via interpersonal context
  • 12-16 sessions, maintenance sessions to avoid relapse
  • work to resolve:
    1) interpersonal disputes
    2) role transitions (life changes)
    3) grief
    4) interpersonal deficits
  • efficacy similar to antidepressants
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187
Q

pharmacotherapy for depression

A

1) TCAs: blocks NE or 5HT reuptake, rarely prescribed because of side effects
2) MAOIs: block MAO, prevents breakdown of NE, 5HT, DA, also rarely prescribed
3) SSRIs: primarily block reuptake of 5HT, more commonly prescribed (minor side effects: nausea, insomnia, sedation, sexual dysfunction)
4) SNRIs: block reuptake for 5HT, NE
5) medications for dopamine (stimulant-like)
6) miscellaneous actions: GABA, ketamine

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188
Q

pharmacotherapy for bipolar disorder

A
  • can’t use antidepressants, these encourage mania
    1) lithium: mechanism unkown (deactivation of GSK-3B? decreasing excitatory glutamate?)
  • narrow therapeutic window means regular blood draws (therapeutic dose is only slightly below toxic)
  • side effects: kidney, thyroid, dehydration, weight gain, hair thinning, hand tremors
  • careful with salt/coffee intake
  • 40% do not respond, becomes ineffective over time for 70%
    2) anticonvulsants: originally for epilepsy
  • mechanism also unknown
  • many increase GABA
  • some decrease glutamate
  • some work on Ca2+ and Na+ channels
    3) atypical antipsychotics: work on dopamine and serotonin, can cause tardive dyskinesia
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189
Q

tardive dyskinesia

A
  • protrusion and rolling of tongue
  • sucking and smacking movements of lips
  • chewing motion
  • facial dyskinesia
  • involuntary movements of body and extremities
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190
Q

combination therapies for bipolar disorder

A
  • medication first choice, but can add adjunct therapy
    1) family-focused therapy (FFT): education for patient and family, communication and problem-solving training, developing positive interactions and supportive relationships
    2) interpersonal and social rhythm therapy (IPSRT): regulation of routines and coping with stressful life events, targets sleep consistency, prevents relapse via sleep deprivation
    3) cognitive therapy (CT): regulate sleep and daily routines, monitor mood for episode triggers, medication compliance
    4) dialectical behavioural therapy (DBT): improve emotional regulation, reduced negative coping, reduced vulnerability to strong emotions
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191
Q

phototherapy

A
  • useful in SAD
  • light boxes emit a bright light of a certain intensity to mimic sunlight
  • patients sit in front of box for 30 min in morning
  • increasing temperature, serotonin production, melatonin inhibition
  • no side effects, <100 dollars
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192
Q

treatment-resistant depression

A
  • 40% fail to respond to at least two medications
  • consider neurosurgery
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193
Q

neurosurgery and invasive procedures for depression

A

1) ECT: used for severe and treatment-resistant cases, remission rate ~90%
2) TMS: usually applied to DLPFC (dorsolateral prefrontal cortex) where there is low activity, less effective than ECT
3) vagus nerve stimulation (VNS): invasive, helps improve 5HT/NE and blood flow, works well in long-term
4) DBS: extremely invasive electrodes in reward/attention areas

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194
Q

suicide stigma

A
  • cultural and religious views impact prevalence
  • wasn’t considered “legal” in some countries
  • stigma prevents people from seeking help
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195
Q

dialectical behavioural therapy

A
  • built to treat suicidality, although common for BPD
  • emphasizes that wo things can be true at the same time
  • aims for a balance between acceptance (mindfulness, distress tolerance) and change (emotional regulation, interpersonal effectiveness)
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196
Q

different types of suicidal behaviour

A

1) ideation: thoughts of death, thinking of ways it could happen
2) gestures (parasuicide): behaviours that look like a suicide attempt but are not life-threatening/have no intention
3) attempts: carrying out a plan
4) completion: successful attempt
5) self-harm

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197
Q

self-harm

A
  • not immediately life-threatening
  • maladaptive ways of coping
  • negative reinforcement: intense release/relief after (attentional shift)
  • strong predictor of suicidal behaviour or mood disorder
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198
Q

DBT treatment for self-harm

A
  • behaviour chain analysis
  • look at precursors to self-harming behaviour and try to intervene sooner rather than letting feelings escalate
  • teach emotional regulation, mindfulness
  • avoid situational/emotional triggers
  • take focus away from painful feelings
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199
Q

schizophrenia general characteristics

A
  • disruption of basic psychological processes
  • distorted perception of reality
  • altered/blunted emotion
  • disturbances in thought, motivation and behaviour
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200
Q

schizophrenia prevalence, onset, demographics

A
  • prevalence: 1%, 300k in Canada
  • onset: 15-45 years, early 20s peak
  • men/women roughly equal risk, men develop earlier
  • abrupt or gradual onset
  • all socioeconomic levels, but more prevalent at low (self-fulfilling prophecy, comorbidities with depression, suicidality, substance abuse)
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201
Q

most common type of hallucinations

A

auditory

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202
Q

complexity of schizophrenia

A
  • heterogenous in terms of symptoms
  • no reliable biological markers
  • difficult to make prognosis and prediction
  • what defines successful treatment? symptoms gone or disruption gone?
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203
Q

factors increasing schizophrenia prevalence

A
  • industrialization
  • rural vs urban living
  • environmental changes
  • defined disorder = more diagnoses
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204
Q

schizophrenia prognosis

A
  • poorer for males and those with earlier onset
  • chronic and relapsing disorder
  • longer delay for treatment worsens prognosis
  • favourable outcome: typically termed attenuated psychosis rather than in remission (most cases, symptoms still present, just less intense)
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205
Q

schizophrenia burden on society

A
  • economy: billions of dollars on inpatient services, psychiatric case management, much more direct and frequent client care required
  • stigma
  • family members usually have to act as caregivers, extra loss of productivity
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206
Q

division of symptoms in schizophrenia

A

1) positive: something extra present, ex. hallucinations, delusions, disorganized speech and thoughts
2) negative: something absent or abnormal, ex. ahedonia, avolition (lack of motivation to start a task), blunted afect
3) cognitive: dysfunction in brain’s regular processes, ex. memory issues, inability to process social cues, impaired sensory perception

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207
Q

hallucinations

A
  • realistic perceptions in the ABSENCE of external sensory input that occur while awake and conscious
  • underlying problem: misattribution of sensory experience and inability to discriminate between internal/external sources of information
  • occur in many medical disorders, and does not necessarily mean psychotic
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208
Q

types of hallucinations

A

1) auditory: heard inside or outside of head
2) visual: simple or complex, cannot be an illusion or misinterpretation of existing stimulus
3) tactile
4) taste or smell: often extreme

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209
Q

delusions

A
  • implausible beliefs that persist despite reliable contradictory evidence
  • disorder of thought content
  • can include complex belief system or single belief
  • observed correlation: may develop in people who make interpretations too quickly and jump to conclusions
  • may also be a bias in reasoning (negative events always perceived as coming from environment or other people)
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210
Q

types of delusions

A

1) persecutory/paranoid: they are being conspired against, deceived or persecuted
2) referential: events, objects or other individuals have personally relevant meanings
3) somatic: change or disturbance in personal appearance or bodily function
4) religious: unusual religious experiences or beliefs, ex. describing self as living out a biblical prophecy
5) grandiose: possession of special or divine powers, abilities or knowledge

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211
Q

motor disruptions

A
  • catatonia: reduction in motor responsiveness
  • waxy flexibility: allowing others to move their body and limbs, then maintain that position
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212
Q

grossly disorganized behaviour

A
  • difficulty with goal-directed behaviour
  • unpredictable movements
  • problems dressing or with hygiene
  • inappropriate sexual behaviour
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213
Q

negative symptoms associated with…

A

deficits in academic and occupational functioning and adjusting to community

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214
Q

disorganized speech and thought disorder

A
  • unusual-sounding, nonsensical speech
  • loosening of associations: loss of logical connections between ideas
  • tangential thinking: moving from one topic to another quickly
  • more easily observable, can serve as objective index of disturbance (over symptoms like hallucinations and delusions)
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215
Q

cognitive deficits as markers of schizophrenia

A

1) processing speed: slow writing symbols paired with numbers
2) sensory gating: impairment filtering out redundant info
3) verbal memory
4) dichotic listening
5) phonemic word fluency: impaired generation of words rapidly
6) ability to sustain attention: slow/inaccurate detection of specified letters

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216
Q

progression of schizophrenia

A

1) premorbid
2) prodormal: clinical deterioration begins, 5-10 years before first episode
3) progression/clinical deterioration: longer period of untreated psychosis = worse prognosis, number of relapses related to greater deterioration
4) chronic residual: patients may not recover from subsequent episodes as quickly, may experience greater degrees of residual symptoms and disability

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217
Q

schizophrenia DSM criteria

A

1) two or more of following, each present for a significant portion of time during 1 month:
- delusions
- hallucinations
- disorganized speech
- grossly disorganized or catatonic behaviour
- negative symptoms
2) for significant portion of time since onset, level of function in one or more areas is below level prior to onset (work, interpersonal, self-care)
3) continuous signs of disturbance persist for at least 6 months: includes at least 1 month of symptoms (less if treated), may include periods of prodromal or residual symptoms (only negative symptoms or two or more symptoms with attenuated form)
4) rule out schizoaffective disorder, MDD or BP with psychotic features
5) not attributable to substance, medication or medical condition
6) if autism or communication disorder present, diagnosis can only be given if delusions or hallucinations present for one month (less if treated)

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218
Q

delusional disorder

A
  • one or more delusions with duration of one month or more
  • does not meet criteria for schizophrenia (never been met)
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219
Q

brief psychotic disorder

A
  • one or more of: delusions, hallucinations, disorganized speech, grossly disorganized/catatonic behaviour
  • at least one symptom from first three categories
  • 1 day to 1 month, more becomes schizophreniform disorder
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220
Q

schizophreniform disorder

A
  • two or more of symptoms: delusions, hallucinations, disorganized speech, grossly disorganized/catatonic behaviour, negative symptoms
  • at least one from first 3
  • 1 month to 6 months, more becomes schizophrenia
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221
Q

schizoaffective disorder DSM criteria

A

1) two or more symptoms, each present for significant amount of time during 1-month period + at least one from first three:
- delusions
- hallucinations
- disorganized speech
- grossly disorganized or catatonic behaviour
- negative symptoms
2) hallucinations and delusions for two or more weeks in the absence of a major mood episode during entire life time duration of illness
3) symptoms that meet criteria for major mood episode are present for the majority of the time otherwise (including active and residual portions of illness)
4) not due to substance or medical condition
5) specifiers:
- bipolar type: mania and sometimes major depression
- depressive type: only major depressive episodes

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222
Q

substance/medication-induced psychotic disorder

A

ex. cannabis

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223
Q

other specified psychotic disorders

A
  • persistent auditory hallucinations (+ nothing else)
  • delusions with significant overlapping mood symptoms
  • attenuated psychosis syndrome (below threshold)
  • psychotic disorder - not otherwise specified (NOS)
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224
Q

MDD + psychotic features vs schizoaffective disorder

A
  • MDD with PF only experience psychotic features during mood episodes
  • schizoaffective have 2 weeks only psychotic symptoms without mood symptoms
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225
Q

bipolar disorder vs schizoaffective disorder

A

same distinction as MDD with PF

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226
Q

neuropsychological and neuroimaging factors in schizophrenia

A
  • suggest hypofrontality, affecting personality, self-awareness, motivation, thinking, impulsivity, social behaviour
  • can predict schizophrenia or indicate severity, but cannot diagnose
    1) fMRI: less than 50% have reduced blood flow or metabolism in frontal area during tasks
  • schizophrenia could be a product of lower intellectual functioning overall (50-67% lower in patient groups)
    2) MRI: third and lateral ventricles are enlarged (compression or loss of existing nerve tissue)
  • reduced grey matter volumes in medial temporal lobe (MTL), superior temporal lobe, prefrontal cortex –> memory processing, cognitive/executive function (but not in all patients)
    3) DTI: corpus callosum and connections between frontal lobe and other areas affected (connective tissues and tracts)
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227
Q

social cognition factors in schizophrenia

A
  • emotional recognition (six universal) decreased (index of social functioning)
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228
Q

biological factors in schizophrenia

A

1) high genetic contribution: children of two affected parents = 35% likelihood
- molecular genetics research difficult to reproduce consistently
- single gene only increases risk by 1-1.5% because of many interactions
2) pregnancy/birth: mother exposure to flu or illness, birth-related complications
3) family environment: family hostility, lack of support, critical attitudes, over-involvement, mood/eating disorders, high expressed negative emotion directed at family members with disorder
4) other factors: high-risk children display withdrawn/socially-reclusive, antisocial, aggressive behaviour, motor difficulties, lower intellectual capabilities

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229
Q

psychoanalytic etiology of schizophrenia

A
  • emotional traumas
  • inadequate parenting
  • severely rejecting mother: schizophrenogenic
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230
Q

sociocultural etiology of schizophrenia

A
  • strong correlation with poverty
  • social drift: people from lower SES get stuck bc of reduce IQ associated, more substance use, stigma, homlessness
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231
Q

diathesis-stress model in schizophrenia

A
  • popular explanation
  • biological vulnerability (inherited or acquired early in life) switched on by stress
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232
Q

meehl’s model

A
  • most famous for schizophrenia
    1) hypokrisia: biological diathesis that causes nerve cells to be abnormally reactive to incoming sensory info (can be suppressed by other genes)
    2) cognitive slippage: information is disorganized, incoherent and scrambled, increases thought disorder risk (high IQ can prevent further progression)
    3) aversive drift: negative symptoms from unpleasant social experiences that amplify pain, weaken pleasure and make social relationships difficult
    4) schizotype: has all three predispositions, can still be spared
    5) schizophrenia: more likely with exacerbating factors: shyness, anxiety, low energy, weak motivation, low ability, talent, low SES
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233
Q

criticism for meehl’s model

A
  • complicated (not parsimonious)
  • lacks integration of why disorder emerges in adolescence
  • lack of empirical support for only three specific factors
  • subtle brain injuries present in areas that normally mature in adolescence may be important –> stress of maturation on weakened brain, hormonal interaction with stress
  • overall, neuroanatomical and neurochemical theories are more evolved
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234
Q

dopamine hypothesis in schizophrenia

A
  • abnormal concentrations of dopamine receptors
  • key medication: chlorpromazine blocks dopamine receptors (D2)
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235
Q

mesolimbic pathway in SCZ

A
  • reward and regulation
  • too much signaling = hallucinations/delusions
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236
Q

mesocortical pathway in SCZ

A
  • emotional and cognitive functioning, executive functions
  • too little signaling = negative/cognitive symptoms (hypofrontality)
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237
Q

historical treatments for SCZ

A

insula coma, psychosurgery, frontal lobotomies, shocks

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238
Q

typical antipsychotics

A
  • dopamine receptor antagonists
  • ex. chlorpromazine: reduced agitation, mania, mood disturbances (positive symptoms)
  • may exacerbate negative/cognitive symptoms
  • minority benefit, others have side effects
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239
Q

nigrostriatal pathway in SCZ

A
  • coordinated movement
  • normal signaling
  • typical antipsychotics = low signaling = parkinsonian symptoms
240
Q

tuberoinfundivular pathway

A
  • normally dopamine inhibits prolactin
  • typical antipsychotics = low signaling = mammary glands stimulated
241
Q

atypical antipsychotics

A
  • preferred medication for SCZ
  • dopamine and serotonin receptor antagonists
  • ex. risperidone, olanzapine
  • fewer side effects
242
Q

psychotherapy for SCZ

A

more challenging because of complexity, commonly used as adjunct to medication

243
Q

CBT for SCZ

A
  • targets: emotional disturbance, psychotic symptoms, social disabilities, risk of relapse
  • techniques: psychoeducation, normalization of symptoms, belief modification, coping strategy enhancement, reduce catastrophic misinterpretations (symptom management)
  • taught how to interpret relevant environmental events
  • taught to respond appropriately to social cues
244
Q

other treatments for SCZ

A

1) social skills training
2) cognitive remediation and emotion recognition training: improving memory, attention, cognitive ability through compensatory strategies, exercises, group discussions
3) family therapy: emotional communication, problem-solving, stress-related coping skills

245
Q

importance of early access, awareness and prevention in SCZ

A
  • longer untreated = more distress and dysfunction
  • STEPS for youth: early intervention, assessment and treatment for youth with signs and symptoms of psychosis
  • cannabinoids produce symptoms like SCZ, has a dose-related higher risk for psychosis in later life
246
Q

grouping of mental health diagnoses

A

1) internalizing: overcontrolled behaviours, ex. anxiety, depression, OCD, specific phobias
2) externalizing: undercontrolled, ex. oppositional defiant disorder, substance abuse, conduct disorder

247
Q

p factor

A
  • common root of mental health diagnoses capturing about half of variance
  • speculation: roots in emotion dysregulation and negative affectivity
248
Q

what is the importance of the p factor?

A
  • highlights comorbidity as common
  • understanding mental health should be rooted in recognizing overall risk for worsening mental health
249
Q

disruptive behaviour disorders (DBDs)

A
  • difficulty with rule following, impulsivity, aggression and getting in trouble
  • often male
  • oppositional defiant disorder (ODD)
  • conduct disorder (CD)
250
Q

ODD DSM criteria

A

1) at least 4 symptoms on most days for at least 6 months:
- often loses temper
- often touchy or easily annoyed
- often angry and resentful
- often argue with authority figures or adults
- often actively refuse to defy to comply with requests from authority figures or with rules
- often deliberately annoys others
- often blames others for his or her mistakes or misbehaviour
- child has been spiteful or vindictive at least twice within past 6 months
2) evidence of impairment: distress (individual or people around) and/or negative impact on social, educational, occupational or other areas of functioning
3) not attributable to substance use or other disorders
4) patient does not meet criteria for disruptive mood regulation disorder

251
Q

ODD severity

A
  • mild = 1 setting
  • moderate = 2 settings
  • severe = 3 or more settings
252
Q

CD DSM-5 criteria

A

1) four of the following:
- aggressive behaviour towards others and animals
- frequent physical altercations with others
- use of weapon to harm others
- deliberately physically cruel to other people
- deliberately physically cruel to animals
- involvement in confrontational economic order crime
- has perpetrated a forcible sex act on another
- arson
- property destruction
- non-confrontational economic order crime
- non-confrontational retail theft
- disregarded parent’s curfew prior to age 13
- run away from home at least two times
- truant before age 13 (skipping school)
2) significant impairment in functioning
3) if over 18, does not meet criteria for antisocial personality disorder

253
Q

CD and ODD relationship

A
  • highly correlated, can have both at once
  • most children with CD initially display signs of ODD
  • most children with ODD do not go on to have CD
  • separation: CD violates basic rights of others or major societal norms/rules
254
Q

ODD emergence

A
  • 3-9 years
  • often first observed within relational context with caregivers
  • as severity increases, behaviours start to generalize
  • thus, family is main target for intervention, but genetics/environment also at play
255
Q

intervention for DBDs

A

1) parent management training (PMT)
2) CBT for older kids (cognitive capacity, less reliant on parents)
3) multisystemic therapy: work with integrated environmental systems (delivered in natural environment)
*high relational focus!

256
Q

most effective intervention methods for DBDs

A
  • classroom-based
  • family-based
  • limited support for individual-based
257
Q

why is it extra important to treat DBDs?

A
  • early mental health risk
  • cascading downstream risks: APD, depression, anxiety
  • externalizing to internalizing disorder: DBDs cause a lot of peer isolation and decreased well-being
258
Q

patterns of anxiety (GAD) over age

A
  • U-shaped curve: decrease in middle-childhood, increases in adolescence
  • females higher rates of anxiety only after 15+
259
Q

patterns of separation anxiety over age

A
  • common in middle childhood, basically disappears by early teens
  • makes sense: first starting school, then get used to it
260
Q

connecting separation anxiety to generalized anxiety

A
  • generalized repeaks starting when separation ends
  • anxiety manifests itself differently
261
Q

patterns of depression over age

A
  • starts earlier in girls
  • low in childhood, increases around 13
  • 15-18: rates peak, but level off and stabilize throughout adulthood
262
Q

why are trajectories important?

A
  • better normalize symptoms and decrease stigma
  • early mental health complications are relatively normal and expected
263
Q

what do we learn from mental health prevalence studies?

A
  • mental health seems to follow life-course perspective
  • mental health diagnoses affect nearly everyone
  • mental health diagnoses are not stable
  • comorbidity is common and expected
  • mental health complications are not rare or stigmatizing, but should be expected
264
Q

homotypic continuity

A

single diagnosis predicting the same diagnosis over time

265
Q

heterotypic continuity

A

single diagnosis predicting risk for a separate diagnosis

266
Q

early life adversity (ELA)

A
  • one of the most common psychosocial risk factors for development or worsening of mental health complications and increased treatment resistance
  • disproportionate effect on minority racial/ethnic groups and lower SES
  • dose-dependent relationship
  • one adverse childhood experience increases odds of another
267
Q

relational health model

A
  • shift from medical symptom management/treatment to relationships and community support
  • preventative medicine: recognizing that good wellbeing starts with early life experiences
  • resilience based on interconnected systems of social support
268
Q

autism spectrum disorder (ASD) prevalence and etiology

A
  • 1% worldwide
  • huge increase in prevalence recently (from 1 in 2222)
  • highly heritable (40-80%)
269
Q

ASD features

A

1) persistent impairment in reciprocal social communication and social interaction
2) restricted, repetitive patterns of behaviour, interest or activities
3) symptoms present from early childhood
4) symptoms impair everyday functioning

270
Q

ASD and gender

A
  • diagnosed 4x more often in males
  • girls with ASD at risk of being overlooked, mislabeled or identified later
  • could be related to different presentation in girls than boys
271
Q

ASD diagnostic measures

A
  • early developmental screening: checklists, surveys, lack of eye contact and not responding to name
  • parent-based interview
  • direct observation of behaviours across different play-based scenarios
272
Q

ASD identity-first language

A
  • conflict between identity-first and person-first, generally better to ask individual’s preference
273
Q

ASD intervention (therapies)

A
  • applied behaviour analysis (ABA): focused on behaviour management –> teach social, motor, behaviour and reasoning skills
  • parent training encouraged to model behaviours at home
  • early intensive behavioural intervention programs (EIBI)
274
Q

issues with ABA/EIBI

A
  • lack of autonomy and involvement + pressure to conform to standards of typicality
  • movement towards naturalistic developmental behavioural interventions: natural settings, involve child, teach developmentally appropriate skills, ex. social ABCs: parent-mediated program to help with social-communication challenges
275
Q

ASD intervention (communication)

A

1) picture exchange communication system (PECS): communication through specific symbols
2) speech generating devices (SGD): portable devices that produce speech when visual graphics selected –> may be less stigmatizing to use device

276
Q

ASD intervention (self-regulation)

A
  • principles of mindfulness to help with complications with self-regulation
277
Q

ADHD prevalence and etiology

A
  • 8% in children and adolescence globally
  • strong genetic basis (74-80%)
  • DSM-5 biological basis: brain-based developmental disorder)
278
Q

ADHD diagnostic criteria

A

1) inattention: 6+ for <16, 5+ for 17+, symptoms present for at least 6 months and inappropriate for developmental level
- often fails to give close attention to details, makes careless mistakes
- often has trouble holding attention
- often does not seem to listen when spoken to directly
- often does not follow through on instructions or responsibilities
- often has trouble organizing tasks/activities
- often avoids, dislikes or is reluctant to do tasks that require mental effort over a long period of time
- often loses things necessary for tasks/activities
2) hyperactivity and impulsivity: same as 1)
- often fidgets, taps hands or feet, squirms in seat
- often leaves seat in inappropriate situations
- often runs around our climbs inappropriately (adolescents/adults = restless)
- often unable to play or take part in leisure activities quietly
- often “on the go” as if “driven by a motor”
- often talks excessively
- often blurts out an answer before question completed
- often has trouble waiting their turn
- often interrupts or intrudes on others

279
Q

ADHD classifications

A

1) ADHD-I: predominantly inattentive presentation
2) ADHD-H: predominantly hyperactive/impulsive presentation
3) ADHD-HI: combined presentation

280
Q

ADHD classification gender differences

A
  • ADHD-I more common in girls, associated with greater difficulty in school achievement (particularly math)
  • ADHD-H and AHDH-HI 3x more common in boys, associated with greater conduct problems
281
Q

ADHD treatment

A

1) stimulant medication: effective in 80% of children (different medication in children vs adults)
2) parent psychoeducation: understanding symptoms and building strength-based approaches within the home
3) academic skill intervention
4) behavioural parent training
*no strong evidence to suggest benefit of family, individual or social skills therapy

282
Q

ADHD diagnostic measures

A

*no one objective test can confirm or rule out ADHD, important to get comprehensive assessment
1) Conner’s Rating Scale for ADHD (self-report, parent or teacher)
2) semi-structured interview
3) performance-based measures to gather evidence
4) additional data: report cards, comorbid diagnoses

283
Q

specific learning disorders (LDs)

A

persistent impairment in one of three major areas:
1) dyslexia (reading): connecting written letters to sounds, difficulties with phonemic awareness or rapid automatized naming
2) dysgraphia (written expression): thoughts to paper, difficulties with executive function, physical act of writing, common conventions of writing
3) dyscalculia (math): difficulty with number-related concepts or mathematical symbols

284
Q

why is DSM-5 not used for learning disabilities?

A
  • mainly requires documented academic impairment
  • does not tell us how learning is impaired
285
Q

learning disability (LDAO guidelines)

A

1) demonstrated impairment in academic achievement
2) evidence of psychological process underlying challenges
3) at least average abilities essential for thinking/reasoning
4) not better accounted form for other factors

286
Q

LD prevalence rates

A
  • difficult to define because of variations in criteria
  • affects girls/boys equally
287
Q

LD comorbidities

A
  • individuals with LDs 2-3 times more likely to experience mental health complications
  • feelings of failure, stress of needing to fit in/appear normal, reduced sense of competency/self-efficacy compared to peers
288
Q

LD intervention

A
  • multi-tiered framework:
    1) full population screened for (ex. reading) ability
    2) strategies taught to “at-risk” students for reading difficulties
    3) those not responsive receive additional intense remediation support
289
Q

LD diagnostic measures

A

1) comprehensive test of phonological processing
2) measures of academic achievement
3) visual motor integration test (graphomotor abilities)

290
Q

simple view of reading

A

strong word recognition skills + comprehension of language = strong reading comprehension

291
Q

problem with simple view of reading

A
  • this is not how reading is usually taught
  • balanced reading curriculum (3 cueing method: context cues encouraged, phonics discouraged (boring)
292
Q

components of an emotional experience

A

1) stimulus
2) cognitive: alterations in consciousness and specific thoughts
3) physiological: autonomic nervous system changes
4) behavioral: behaviour change
5) emotion = subjective experience

293
Q

anxiety, fear, panic (differences)

A
  • anxiety = affective (emotional) state where someone feels threatened by the POTENTIAL occurrence of a FUTURE negative event
  • fear = response to real or perceived threat in the present, elicits fight or flight response
  • panic = rapid physiological response (like an “alarm” that can be triggered in absence or presence of a concrete, identifiable event
294
Q

the “anxiety equation”

A

predicted likelihood of threat / predicted ability to cope

295
Q

historical perspective on anxiety disorders

A
  • neurosis: implied biological explanation, used to be classified with dissociative and somatoform disorders
  • Freud: repressed inappropriate thoughts caused neurotic anxiety
  • modern views: cognitive, behavioural, biological factors combined with environmental
296
Q

genetic etiology of anxiety disorders

A
  • some heritability (23-40%)
  • risk in the bform of temperamental and dispositional traits:
    1) behavioural inhibition: likelihood of shyness/withdrawal from unfamiliar situations
    2) neuroticism
  • environmental influence shown to be more important
297
Q

biological (neurotransmitter) etiology of anxiety disorders

A
  • serotonin, norepinephrine, GABA
  • benzodiazepines enhance GABA, decreases anxiety
298
Q

behavioural etiology of anxiety disorders

A
  • classical and operant conditioning (two-factor theory)
  • social learning variants (vicarious learning)
299
Q

cognitive/attentional etiology of anxiety disorders

A
  • anxious schemas + belief that one will not be able to cope
  • core beliefs of helplessness and vulnerability
  • bias in information processing: eye-tracking procedures show that they tend to focus on negative information (even in faces)
300
Q

interpersonal/social learning etiology of anxiety

A
  • parents with anxiety: less warm, more critical, less granting of autonomy
  • parenting style may foster beliefs related to helplessness and uncontrollability (internal working model: self as worthy/unworthy of care and others as reliable/unreliable sources of support)
  • anxious-ambivalent attachment may predict anxiety
301
Q

Barlow’s triple vulnerability model

A

1) genetic predisposition
2) non-specific psychological factors (ex. general low self-esteem, feeling lack of control)
3) specific psychological factors (ex. x is a threat, worrying is dangerous, threats must be avoided)
- all lead to clinically significant psychological disorder

302
Q

diagnostic organization of anxiety disorders in DSM-5

A

1) anxiety disorders: panic disorder, agoraphobia, SAD, specific phobia, GAD
2) obsessive-compulsive and related: OCD, body dysmorphic disorder, hoarding disorder, etc.
3) trauma and stressor related: PTSD, acute stress, adjustment, etc.

303
Q

panic attack criteria

A

sudden rush of intense fear/discomfort, peaks at 10 mins with 4/13 of:
- heart palpitations or accelerated heart rate
- sweating
- trembling or shaking
- shortness of breath
- feelings of choking
- chest pain or discomfort
- nausea or abdominal distress
- dizziness, unsteady, light-headed or faint
- chills or hot flashes
- numbness or tingling
- derealization or depersonalization
- fear of losing control or going crazy
- fear of dying

304
Q

panic disorder general characteristics

A
  • panic attacks do not equal panic disorder!
  • women twice as likely
  • treatment usually sought years after occurrence, when symptoms get “bad enough”
  • often comorbid with other disorders
305
Q

panic disorder DSM-5 criteria

A

1) recurrent and unexpected panic attacks (at least two), peak within minutes, meeting criteria for panic attack
2) at least one attack followed by 1+ month of one or both:
- persistent concern or worry about additional attacks or their consequences
- significant maladaptive change in behaviour related to the attacks
3) not attributable to substance or medical condition
4) not better explained by other psychological disorders

306
Q

alarm theory

A
  • system activated by emotional cues, creates false alarms, triggers panic attacks in neutral situations with absence of threat
    1) trigger
    2) perceived threat
    3) apprehension
    4) body sensations
    5) physical/cognitive anxiety sensitivity –> physical/mental catastrophic misinterpretation <–> panic self-efficacy decreases
    6) loop back to perceived threat
307
Q

agoraphobia general characteristics

A
  • anxiety about being in places or situations where it is difficult to escape or where help is not readily available should a panic attack occur
  • highly comorbid with PD, but agoraphobia can be present without PD
  • avoidance and safety behaviours
308
Q

how to safety behaviours contribute to disordered anxiety?

A

validate the fear

309
Q

agoraphobia DSM-5 criteria

A

1) marked fear or anxiety about 2+ situations:
- using public transportation
- being in open spaces
- being in enclosed spaces
- standing in a line or being in a crowd
- being outside the home alone
2) fear or avoidance of above because of thoughts that escape is difficult or help might not be available in the event of panic-like symptoms or other incapacitating/embarrassing symptoms
3) agoraphobic situations almost always provoke fear or anxiety
4) agoraphobic situations actively avoided, require presence of companion or are endured with intense fear/anxiety
5) fear/anxiety out of proportion
6) 6+ months persistence, clinically significant distress or impairment, no medical/substance/other condition explanation

310
Q

PD/agoraphobia assessment

A
  • semi-structured interview
  • behavioural measurement
  • psychophysiological tests
  • self-report measures, ex. behavioural avoidance test (BAT): rating degree of anticipatory anxiety and actual level of anxiety in various situations
  • rule out medical conditions (hypoglycemia, hyperthyroidism)
311
Q

PD/agoraphobia genetic etiology

A
  • no specific genes
  • increased susceptibility to biological challenges, ex. subtle increases in CO2
  • higher occurrence of nocturnal panic (waking up with panic attack)
312
Q

cognitive model of PD/agoraphobia

A

1) physiological trigger or sensation
2) cognitive evaluation: threat perceived
3) cycle: anxiety, intensifying 1) because of intentional focus, catastrophic misinterpretation
4) safety/escape behaviours contribute to catastrophic misinterpretation

313
Q

specific phobia general characteristics

A
  • marked and persistent fear/avoidance of specific objects or situations
  • excessive, disproportionate fear
  • significant interference with life
314
Q

specific phobia subtypes/specifiers (5)

A

1) animal
2) natural environment
3) blood-injection-injury (bodily harm, medical treatment)
4) situational
5) other

315
Q

specific phobia prevalence

A
  • 12.5% in past year, 18.4% lifetime
  • women almost 2x higher, with subjectively greater degree of fear
  • women typically report phobias of animal and situations
  • genetic heritability 35-51%
  • fear of animals most common
316
Q

specific phobia DSM-5 criteria

A

1) marked fear/anxiety about a specific object or situation
2) phobic subject almost always provokes immediate fear/anxiety
3) phobic subject actively avoided or endured with intense fear/anxiety
4) fear/anxiety out of proportion to actual threat and sociocultural context
5) fear/anxiety/avoidance is persistent, lasting 6+ months
6) fear/anxiety/avoidance causes clinically significant distress or impairment
7) not explained by other mental disorders

317
Q

etiology of phobias

A

1) classical/operant conditioning
2) non-associative model
3) biological preparedness theory
4) disgust sensitivity

318
Q

criticism of classical/operant conditioning explanation for phobias

A

equipotentiality premise: everything should then have an equal chance to have a phobia for, not true

319
Q

non-associative model

A
  • evolutionarily equipped to fear certain stimuli over others
  • phobias exist to start out
  • explains infant stranger anxiety
  • most people habituate to feared stimuli, unless they do not have enough exposure to object/situation
320
Q

biological preparedness theory

A
  • natural selection equips us with potential to develop phobia of objects/situations that presented threats to our species over time
  • associative learning still required to develop the phobia in this theory
321
Q

disgust sensitivity

A
  • may be involved in specific phobias and OCD moreso than other anxiety disorders
  • how susceptible to being disgusted by variety of stimuli
  • people not just afraid of things, but appraise the object as being able to do disgusting things
  • may be important treatment outcome (decreasing this correlated with decreasing phobia)
322
Q

social anxiety disorder general characteristics

A
  • distinguished from general shyness: intensely afraid of social and/or performance situations
  • fear showing signs of anxiety or worry that they will behave in a socially inept way and then be judged or criticized
  • interpersonal disorder
  • late childhood/adolescence onset
323
Q

SAD genetic etiology

A
  • genetic factors ~50%, behavioural inhibition (temperament)
324
Q

SAD biological etiology

A

brain structures:
- fear recognition and conditioning involved (amygdala)
- anxious arousal/stress (HPA axis, dysregulation of serotonin, NE, etc.)
- tendency to monitor own neg. affect (prefrontal, orbitofrontal cortex)

325
Q

SAD environmental factors

A
  • victimization during childhood (linked to dysregulated HPA axis)
  • intrusive and overprotective parents
326
Q

SAD cognitive factors

A
  • neg. beliefs about self and others (dishonest self-disclosure)
  • abnormal or biased processing of social info
  • high threat monitoring
  • high self-consciousness
327
Q

SAD and social skills

A
  • actual deficit in skills leads to self-perpetuating interpersonal cycle
  • avoidance and eventual peer rejection = further anxiety and depression
328
Q

SAD DSM-5 criteria

A

1) marked fear/anxiety about 1+ social situations in which individual is exposed to possible scrutiny by others (social interactions, being observed, performing)
2) fear that they will act in a way or show anxiety symptoms that will be negatively evaluated
3) social situations almost always provoke fear/anxiety
4) social situations avoided or endured with intense fear/anxiety
5) fear/anxiety acknowledged as out of proportion to actual threat and sociocultural context
6) persistent (6+ months), clinically significant distress/impairment, not attributable to substances, medications, other disorders
*if medical condition present, fear/anxiety/avoidance is unrelated or excessive

329
Q

GAD risk factors and role of cognition

A
  • intolerance of uncertainty:
    1) trigger: novelty, ambiguity, unpredictability
    2) uncertainty
    3) catastrophic misinterpretation of uncertainty
    4) worry <-> anxiety <-> safety behaviours
330
Q

how does worry act as negative reinforcement in anxiety?

A
  • verbal aspects of worry dampen arousal in short-term
  • worrying becomes learned behaviour
331
Q

when is worrying common (i.e. not pathological)?

A

1) specific things rather than most/many things
2) intensity of worry matches situation
3) linked to functional problem solving and belief that you can cope with the outcomes

332
Q

GAD prevalence

A

9% lifetime, more common in females

333
Q

GAD DSM-5 criteria

A

1) excessive anxiety/worry occurring more days than not for 6+ months about a number of life areas
2) hard to control the worry
3) anxiety/worry associated with 3+ symptoms, with at least some following 1)
- restlessness or feeling keyed up/on edge
- easily fatigued
- difficulty concentrating, mind going blank
- irritability
- muscle tension
- sleep disturbance
*a lot of overlap with depression!
4) clinically significant distress or impairment, not attributable to substance/medication/other disorder

334
Q

GAD pharmacotherapy treatment

A

1) older: benzodiazepines (GABA enhancer) –> non-specific effect, risk of dependency, acts as negative reinforcement, counteracts CBT
2) older antidepressants: MAOIs, TCAs –> lower use because of side-effects
3) newer antidepressants: SSRIs, SNRIs, NDRIs –> most well-researched and prescribed

335
Q

GAD CBT techniques

A
  • focus on managing thoughts and behaviours (often have faulty thinking: overestimating risk, probability and severity of threats and underestimating ability to cope)
  • socratic questioning and collaborative empiricism
  • thought record, behavioural experiments
  • notice and limit safety behaviours
  • classify worries as productive (engage and problem solve) and unproductive (welcome/tolerate short-term anxiety on purpose)
336
Q

thought reacords

A

1) situation
2) feelings
3) automatic thoughts
4) case for thoughts
5) case against thoughts
6) alternative balanced thought
7) re-rate moods

337
Q

GAD exposure techniques

A

1) systematic desensitization: unlearning association by pairing relaxation response with feared stimulus (counter-conditioning and extinction)
2) contemporary: approaching anxiety-provoking situations and experiencing anxiety on purpose without engaging in safety behaviours –> body learns the anxiety itself isn’t dangerous and situation is not a threat

338
Q

flooding vs gradual habituation

A
  • exposure to most extreme right away = flooding
339
Q

exposure techniques

A

1) in vivo exposures: real life situations, images, videos, VR = phobias, panic, SAD, GAD
2) imagery exposure (using imagination): GAD, PTSD
3) exposure and response prevention: choosing not to respond with compulsive behaviour (OCD, BDD)
4) interoceptive exposure: induce bodily sensations (panic/SAD)

340
Q

exposure hierarchy

A
  • gradual habituation
341
Q

single session exposure

A
  • flooding
342
Q

SUDs

A

subjective units of distress

343
Q

other techniques for GAD

A
  • social groups
  • pet therapy
344
Q

overall treatment choices for PD, specific phobia, SAD, GAD

A

1) PD: CBT, then SSRIs/anxiolytics (anti-anxiety drugs)
2) SP: in-vivo exposure, CBT
3) SAD: group CBT, regular CBT, medications (ex. propanolol, a beta-blocker)
4) BAD: CBT, them medications (sometimes combined)

345
Q

obsessions in OCD

A
  • recurrent, intrusive and uncontrollable thoughts, impulses or ideas that the individual finds disturbing and anxiety-provoking
  • can be about: uncertainty, sexuality, violence/harm, contamination, religion, perfection, relationships
346
Q

compulsions in OCD

A
  • repetitive behaviours or mental acts that a person performs to reduce anxiety/distress caused by obsession or a feared outcome
  • rigid guidelines
  • don’t always have logical connection to obsession
347
Q

rituals

A
  • action performed repeatedly and/or according to some set pattern
  • ex. handwashing, cleaning, ordering: common because contamination is easy to worry about and address
  • ex. repeated checking, reassurance seeking
348
Q

neutralizations

A
  • brief, usually covert behaviours or mental acts performed to “undo” or “negate” the obsessive thought
  • ex. thinking about being health, someone’s safety, happy memories
  • ex. adding “not” to obsession
  • counting thoughts
349
Q

OCD DSM-5 criteria

A

1) presence of obsessions, compulsions or both (obsessions without compulsions is rare)
- obsessions: a) recurrent or persistent thoughts, urges or images that are intrusive or unwanted and cause distress/anxiety b) attempts to suppress, ignore, or neutralize with some other thought or action
- compulsions: a) repetitive behaviours or mental acts that the individual feels compelled to perform in response to an obsession or rules b) used to prevent or reduce anxiety, or prevent event/situation, ad are clearly excessive
2) obsessions or compulsions are time consuming (>1hr/day) or cause clinically significant distress/impairment
3) symptoms not attributable to substance or medical condition
4) not better explained by other disorders
*no minimum amount of time!

350
Q

insight in OCD

A
  • continuum ranging from poor (lack of awareness) to good (being fully aware of potential absurdity of symptoms)
  • added as a specifier to diagnosis
351
Q

OCD genetic basis

A
  • strong heritability ~50%
352
Q

OCD and mental processing

A
  • dysfunction in frontal cortex prevents processing and organizing relevant info
  • distracted by irrelevant details
  • poor self-monitoring (ritual/worry blurry memory)
  • unable to initiate appropriate behaviour change
  • linked to 5-HT dysregulation, but not fully understood
353
Q

OCD and memory confidence

A
  • repeated checking lowers memory confidence, which intensifies doubt and sustains repeated checking
354
Q

OCD cognitive-behavioural model of etiology

A
  • obsessions caused by person’s reaction to their own harmless intrusive thoughts
  • catastrophic misinterpretations (ex. that thought means i am a danger or at fault)
  • unhelpful efforts to control intrusions (ex. thought suppression)
  • disorder initiated and maintained via maladaptive attempts to cope (compulsions) and negative reinforcement of compulsive behaviour
355
Q

role of faulty appraisals in OCD

A
  • self-reinforcing cycle
    1) trigger
    2) intrusive thought
    3) appraisal (needed for anxiety!)
    4) compulsion
    5) relief (neg. reinforcement), which validates 3)
356
Q

examples of appraisals in OCD

A
  • generally: what does the thought mean? why does having the thought matter?
  • only an evil person would think this
  • thinking this means it is likely to happen
  • it is my responsibility to fix this
  • i cannot tolerate not knowing
  • this is likely to happen
357
Q

body dysmorphic disorder

A
  • preoccupation with one or more perceived defects or flaws in their physical appearance (believe it looks ugly, unattractive, abnormal or deformed)
  • perceived flaws not observable or appear slight to others
  • rule out actual disfiguration and general body dissatisfaction
  • individuals spend lots of time thinking, looking at or doing various behaviours to the body part
  • similar to OCD: may have repetitive behaviours or obsessive thinking about the consequence of such a flaw
  • many seek reassurance, treatment or cosmetic surgery
  • high suicide rate
  • mean onset 16-17, equal M/F ratio
358
Q

body dysmorphic disorder DSM criteria

A

1) preoccupation with one or more perceived defects or flaws in physical appearance that are not observable or appear slight to others
2) at some point, individual performs repetitive behaviours or mental acts in response to concerns
3) preoccupation causes clinically significant distress/impairment in social, occupational or other important area
4) preoccupation not better explained by body fat concerns or an eating disorder

359
Q

muscle dysmorphia

A
  • specifier of body dysmorphic disorder
  • more common in males
  • preoccupied by idea that body build is too small or insufficiently muscular
360
Q

hoarding disorder prevalence

A
  • higher for those middle aged or older
  • higher for those with comorbidities
  • highly genetic (~50%)
  • often have experienced major loss
  • poverty is risk factor
  • often present: indecisiveness, avoidance, difficulty planning and organizing tasks, distractability
  • poses a massive health and safety hazard (ex. fires)
361
Q

hoarding disorder DSM criteria

A

1) persistent difficulty discarding or parting with possessions, regardless of actual value
2) difficulty due to perceived need to save the items, there is distress when asked to discard them
3) leads to accumulation of possessions that congest and clutter active living areas, compromising intended use. if becomes uncluttered, by another person
4) causes significant distress/impairment, including maintaining a safe environment for self and others
5) not attributable to medical condition
6) not better accounted for by another mental disorder

362
Q

animal hoarding

A

subtype of hoarding disorder

363
Q

treatment approaches for OCD/BDD

A
  • exposure and response prevention is first choice (CBT)
  • SSRI sometimes in combination, especially for severe cases
  • mindfulness-based approaches helpful for relapse prevention
364
Q

treatment for hoarding disorder

A
  • CBT with motivational interviewing
  • motivational interviewing: helps clients consider how hoarding behaviours fit with their own values and goals in lives, find motivation to change
  • CT: clients explore dysfunctional beliefs about possessions, notice their thoughts and behaviours, assess their validity and accuracy
  • practice letting go: exposure
365
Q

cognitive therapy for OCD

A
  • challenge faulty appraisals, ignore actual content of obsessions!
  • cognitive restructuring via thought records
  • explore false sense of responsibility via responsibility pies
  • examine likelihood or risk of concerns via continuums
366
Q

cognitive therapy for BDD

A
  • learn body image does not = physical appearance
  • evaluate distorted thoughts about one’s own body and the imagined consequences
367
Q

exposure and response prevention (ERP)

A
  • exposure to situations that trigger obsessive thoughts, anxiety and urge to engage in compulsions
  • experience anxiety while it lasts without engaging in any rituals, neutralization, reassurance seeking or safety behaviours
  • extinguishes cycle and/or negative reinforcement of compulsions
  • reduces threat response to trigger or obsessive thought
  • does NOT directly reduce frequency of intrusive thoughts, but this may naturally happen
368
Q

history of PTSD

A
  • syndrome of psychological symptoms after life threatening events
  • WWI: “shell shock” thought to be related to cowardice
  • seen as immoral character flaw
369
Q

what is considered “trauma” in PTSD?

A
  • aka criterion A traumatic event
  • involved one of:
    1) actual or threatened death or serious injury
    2) threat to the integrity of self or others
  • experienced with intense fear, helplessness or horror
  • has the potential to lead to PTSD, but does not guarantee
370
Q

PTSD DSM criteria

A

1) symptoms occur after the exposure of a traumatic event:
- experiencing
- witness
- learn about it happening to a close person (must be violent or accidental)
- repeated/extreme exposure to aversive details (does not apply to media unless work related, needs to be unwilling exposure)
2) 1 or more symptoms involving re-experiencing symptoms
3) 1 or more symptoms involving persistent avoidance
4) 2 or more negative alterations in cognitive function and mood
5) 2 or more hypervigilance symptoms
6) last at least one month
7) significant stress/impairment
8) unrelated to substance or medical condition

371
Q

what does it mean to say that PTSD is a disorder of non-recovery?

A
  • no natural recovery
  • symptoms after trauma are normal, but if they persist and cause distress/dysfunction, it becomes disordered
372
Q

categories of PTSD symptoms

A

1) recurrent re-experiencing of the event
2) persistent emotional or physiological arousal in response to reminders
3) maladaptive changes in thinking patterns and mood
4) hyperarousal and hyperreactivity

373
Q

PTSD gender differences

A
  • women more likely to develop
  • men: events often related to injuries/death, natural disaster, physical attacks, war, being threatened, held captive/kidnapping
  • women: events more often related to rape, sexual molestation, neglect, physical abuse
374
Q

PTSD risk factors

A

1) pre-event: low SES, low education, low IQ, previous psychiatric history, childhood adversity (abuse)
2) post-event: severity of symptoms, lack of social support, additional stressors
3) interpersonal trauma more likely to provoke PTSD
4) high comorbidity
5) abnormalities in brain volume (smaller hippocampus), dysregulated endocrine function (HPA axis/cortisol) –> cause or effect?

375
Q

distinguishing feature of flashbacks

A
  • lose where you are, think you are back in the memory
376
Q

PTSD treatment approaches

A

1) exposure therapy: emphasis on imaginal exposures, can include in-vivo if feasible
2) CBT: cognitive restructuring of maladaptive beliefs (test and examine)
3) medication
4) last resort: invasive treatment options ex. DBS

377
Q

acute stress disorder

A
  • similar to PTSD except duration is 3 days to 1 month after trauma exposure
  • may become PTSD
378
Q

adjustment disorder DSM criteria

A

1) development of emotional or behavioural symptoms in response to identifiable stressor(s) within 3 months of the onset of the stressor
2) symptoms or behaviours are clinically significant, with one or more of:
- marked distress that is out of proportion to the stressor’s severity or intensity, taking into account context and cultural factors
- significant impairment in social, occupational, or other important areas of functioning
3) does not meet the criteria for another mental disorder and is not an exacerbation of a preexisting one
4) do not represent normal bereavement
5) once stress or consequences have been terminated, symptoms do not persist for more than an additional 6 months (if they do, some other unspecified disorder)

379
Q

criticism of adjustment disorder

A
  • maybe too flexible/catch-all
380
Q

adjustment disorder specifiers

A
  • mood or anxiety symptoms
381
Q

history of dissociative and somatic symptoms disorders

A
  • hysteria
  • demonic possession
  • Freud: conversion of anxiety into physical symptoms to avoid internal conflict and responsibilities
382
Q

categories of dissociative disorders

A

1) dissociative amnesia
2) dissociative identity disorder
3) depersonalization/derealization

383
Q

commonalities between dissociative disorders

A
  • severe maladaptive disruptions or alterations of identity, memory and consciousness that are experienced as being beyond one’s control
  • dissociation: lack of normal integration of one or more aspects of psychological functioning (identity, memory, consciousness, sensorimotor, behaviour)
384
Q

dissociative amnesia primary symptoms

A
  • inability to recall significant personal info in the absence of medical/physical impairment
  • more common among psychiatric patients than general public
385
Q

dissociative amnesia DSM criteria

A

1) inability to recall autobiographic info, usually of a traumatic or stressful nature, that is inconsistent with ordinary forgetting
- often localized or selective amnesia for a specific event or events
- OR generalized amnesia for identity and life history
2) symptoms cause significant distress or impairment in social, occupational or other important areas of functioning
3) not attributable to substance, neurological or medical condition
4) not better explained by DID, PTSD, acute stress disorder, somatic symptom or major/mild neurocognitive disorder

386
Q

dissociative fugue

A
  • specifier for dissociative amnesia
  • sudden travel away from home in addition to memory loss
  • can be acute (days) or chronic (months to years)
  • stressful experiences usually act as precipitating factors
  • extremely rare
387
Q

depersonalization

A
  • distinct sense of unreality and detachment from thoughts, feelings, sensations, actions, body
388
Q

derealization

A
  • feelings of unreality and detachment from one’s surroundings
389
Q

depersonalization/derealization disorder

A

1) presence of persistent or recurrent experiences of depersonalization, derealization or both
2) during experiences, reality testing (knowing who you are) remains intact
- if not = flashback or hallucination
3) symptoms cause clinically significant distress or impairment
4) not attributable to substance or medical condition
4) not better explained by other disorders

390
Q

common intervention for dissociation

A
  • grounding: reconnect to senses in present moment
  • acute intervention
391
Q

dissociative identity disorder characteristics

A
  • host, alters and switching (multiple personalities)
  • average diagnostic age = 29-35
392
Q

DID comorbidities

A
  • depression
  • anxiety
  • substance abuse disorder
  • self-injury
  • non-epileptic seizures
393
Q

DID brain regions

A
  • orbitofrontal cortex
  • hippocampus
  • parahippocampal gyrus
  • amygdala
394
Q

DID DSM criteria

A

1) may be self-reported or observed: disruption of identity with two or more distinct personality traits with:
- marked discontinuity in sense of self and agency
- related alterations in affect, behaviour, consciousness, memory, perception, cognition and/or sensorimotor functioning
2) recurrent, significant gaps in recall of everyday events, important personal info, and/or traumatic events (inconsistent with ordinary forgetting)
3) clinically significant distress/impairment
4) not a normal part of broadly accepted cultural or religious practice or pretend play in children

395
Q

danger of memory recovery

A
  • repressed memories are real but clinical approaches to find them are more likely to induce false memory
  • contemporary research: fMRI for true vs false memories
396
Q

DID trauma model of etiology

A
  • diathesis-stress
  • personality traits: high hypnotisability, fantasy proneness, openness to altered states of consciousness
  • dissociation as a defense mechanism for trauma
397
Q

DID and attachment theory

A
  • disorganized attachment as babies = more vulnerable to developing DID
398
Q

DID socio-cognitive model of etiology

A
  • iatrogenic: manufactured or amplified by therapy
  • culture/media influenced (increased) prevalence
399
Q

types of somatic symptom and related disorders

A

1) somatic symptom disorder
2) illness anxiety disorder
3) conversion disorder
4) factitious disorder
*all share predominant focus on bodily concerns –> dysfunction and distress associated with it is the disorder!

400
Q

hypochondriasis

A
  • older concept: preoccupation with fear of having a serious medical disease
  • now split into two other categories: somatic symptom and illness anxiety disorder
401
Q

somatic symptom vs illness anxiety disorder

A
  • somatic: has significant symptoms including pain, can have (or not) a diagnosed illness
  • illness anxiety: no significant bodily symptoms
402
Q

subtypes of illness anxiety disorder

A
  • care-seeking
  • care-avoidant
403
Q

somatic symptom disorder DSM criteria

A

1) 1+ somatic symptoms that are distressing or result in dysfunction
2) excessive thoughts, feelings or behaviours related to the somatic symptom or associated health concerns; at least one of:
- disproportionate and persistent thoughts about the severity of one’s symptoms
- persistently high anxiety about health or symptoms
- excessive time and energy devoted to symptoms or health concerns
3) state of being symptomatic is persistent, typically more than 6 months (although somatic symptoms may come and go)

404
Q

somatic symptom disorder specifiers

A

1) with predominant pain
2) persistent: more than 6 months

405
Q

illness anxiety disorder DSM criteria

A

1) preoccupation with having or acquiring a serious illness
2) somatic symptoms not present OR if present, only mild. if another medical condition is present or high risk, preoccupation is excessive or disproportionate
3) high level of anxiety about health, individual is easily alarmed by personal health status
4) excessive health-related behaviours or maladaptive avoidance
5) at least 6 months, although specific feared illness may change

406
Q

conversion disorder characteristics

A
  • aka functional neurological symptom disorder
  • features:
    1) loss of functioning in body part
    2) no underlying medical abnormality
    3) psychological factors associated with condition
  • viewed as form of dissociative disorder (high comorbidity + high scores of dissociative experiences, hypnotizability, childhood abuse and trauma)
407
Q

conversion disorder DSM

A

1) 1+ symptoms of altered voluntary motor or sensory functioning
2) clinical findings provide evidence of incompatibility between the symptoms and recognized neurological or medical conditions
3) symptom or deficit not better explained by other medical or mental disorder
4) significant distress or dysfunction or warrants medical evaluation

408
Q

factitious disorder characteristics

A
  • aka munchausen syndrome
  • features:
    1) faking symptoms of illness
    2) symptoms include physiological and/or psychiatric
    3) aim to gain sympathy, care and attention
  • conscious of faking (voluntary)
409
Q

distinction between somatic symptom disorders

A

1) involuntary
- physical symptoms = somatic symptom disorder
- neurological symptoms = conversion
- preoccupation with symptoms = illness anxiety
2) voluntary
- wants sick role (abstract goal) = factitious disorder
- wants direct, specific gain = malingering (not a disorder!)

410
Q

factitious disorder DSM criteria

A

1) falsification of physical or psychological signs or symptoms, or induction of injury or disease, associated with identified deception
2) individual presents themself to others as ill, impaired or injured
3) deceptive behaviour evident even in the absence of obvious external rewards
4) behaviour not better explained by other mental disorder

411
Q

etiology of somatic symptom and related disorders

A

1) psychoanalytic: conversion of anxiety associated with unconscious conflicts
2) physiological: HPA axis
3) cognitive: dysfunctional beliefs about illness
4) personality traits
5) early life experiences
6) social learning: adopting the sick role (imitation or by experience)

412
Q

spectrum of eating behaviours

A
  • restriction and control of appetite
  • normalcy
  • lack of control and an excessive appetite (at least some period)
413
Q

why weren’t eating disorders studied until the 1980s (DSM III)?

A
  • cultural changes in 60-70s promoting thin ideal
  • anorexia nervosa was in DSM I but remained very rare
  • bulimia introduced in III
  • binge eating disorder in V
414
Q

early understanding of anorexia nervosa

A
  • 1870s: first described as women who deliberately sought to lose weight
  • other independent descriptions including symptoms like: significant weight loss, slow pulse rate, skin changes, loss of menstruation (perversions of ego, excluded men)
  • differentiated from hysteria
  • one viewed as a form of hysteria –> psychological reactions to food and eating
  • treatment plan: force feeding
415
Q

feeding/eating disorders

A
  • avoidant/restrictive food intake disorder (ARFID)
  • pica
  • rumination disorder
  • anorexia nervosa
  • bulimia nervosa
  • binge eating disorder
  • other specified (formerly EDNOS)
  • unspecified (least informative)
416
Q

ARFID

A
  • pathological “picky eating” leading to nutritional deficiency (distress and dysfunction)
  • most common in children
  • criteria:
    1) disturbance in eating (lack of interest, avoidance based on sensory characteristics, concern about aversive consequences) as manifested by failure to meet appropriate nutritional/energy needs: significant weight loss, nutritional deficiency, dependence on enteral feeding or oral supplements, interference with psychosocial functioning
    2) not better explained by lack of available food or cultural practices
    3) not associated with AN/BN (no evidence of shape/weight concerns)
    4) not attributable to another medical condition or mental disorder
417
Q

pica

A
  • repetitive eating of non-food (no nutritional) substances that leads to distress/dysfunction (ex. danger)
  • ex. ice, dirt, paint chips, clay, paper
  • 1/4 of children, 1/2 of pregnant women
  • patients claim they eat because of cravings, to reduce nausea or because they like the taste
  • could be due to nutrient deficiency
418
Q

rumination disorder

A
  • regurgitation (voluntary or involuntary) and re-chewing of food followed by re-swallowing or spitting out
  • more common in infants and young children, but also observed in adults
419
Q

anorexia nervosa general characteristics

A
  • intense fear of gaining weight or becoming fat (irrational, because despite low weight)
  • restriction: calories or food refusal, may involve rituals
  • compensatory measures after eating (excessive exercise, hyperactivity that also might be due to malnutrition, purging)
  • conflicts between parents/children are common, leading to secretive behaviors
  • disturbance in body image: general dissatisfaction (overall weight or shape is unacceptable or distressing), patients perceive body parts to be bigger than they actually are
  • low self-esteem
  • hypervigilance in assessing their body
420
Q

purging

A
  • behaviors used to maintain weight loss
  • self-induced vomiting
  • laxatives
  • overuse of enemas and diuretics (ex. digestive teas)
421
Q

AN DSM criteria

A

1) restriction of energy intake relative to requirements, leading to significantly low body weight
2) intense fear of gaining weight or of becoming fat, OR persistent behavior that interferes with weight gain, even though at a significantly low weight
3) disturbance in the way which one’s body weight or shape is experienced, undue influence of body weight or shape on self evaluation OR persistent lack of recognition of the seriousness of the current body weight

422
Q

AN subtypes

A

1) restricting: in last 3 months, has not engaged in recurrent binge eating or purging - weight loss is primarily through dieting, fasting and/or excessive exercise
2) binge eating/purging: in last 3 months, has engaged in recurrent binge eating or purging

423
Q

AN changes from DSM IV

A
  • removed amenorrhea criteria
  • males can officially get disorder
424
Q

assessing criterion A for AN

A
  • use BMI to determine severity
  • have to adjust for age, sex, ethnicity
425
Q

binge-eating disorder general characteristics

A
  • typically overweight because NO compensatory ritual
  • weekly objective binges: eating large amount of food in less than two hours, usually perceived as being out of control
  • the most common ED
426
Q

objective vs subjective binge?

A
  • no firm threshold
  • clinician has to decide
  • often, bimodal distribution: binging is well beyond threshold
427
Q

binge eating disorder DSM

A

1) recurrent objective binge eating
2) binge eating episodes are associated with 3+ of:
- eating more rapidly than normal
- eating until uncomfortably full
- eating large amounts even when not physically hungry
- eating alone because of embarrassment
- feeling guilty, disgusted or depressed after
3) marked distress regarding binges
4) binges occur at least once a week for 3 months on average
5) binging not a compensatory behavior as in BN, and does not occur exclusively during course of BN or AN

428
Q

BN characteristics

A
  • binging coupled with compensatory behaviors (fasting, exercise, purging) DESIGNED to prevent weight gain
  • low self-esteem
  • weight and body shape becomes primary variable to self-evaluation
  • social isolation and depression
  • usually normal BMI (harder to detect problem)
  • binge usually associated with physical discomfort and guilt/worry
429
Q

purging in BN

A
  • might alleviate feelings (ex. vomiting to reduce physical discomfort in stomach)
  • has medical consequences: impaired renal function, CV difficulties (ex. arrhythmias)
430
Q

alternative reasons for binges

A
  • escape from self-awareness
  • high expectations of themselves, constant monitoring and failing to meet often unrealistic standards
  • awareness = anxiety, depression = motivation to escape via sensory overload from binging
431
Q

vicious diet cycle

A

1) diet
2) famine response: lose weight from lean muscle and fat, reduced metabolic rate, increase in fat storage
3) fall off
4) feast response: reduced metabolic rate, loss of muscle, regain weight from fat
5) overweight and repeat

432
Q

BN DSM criteria

A

1) recurrent episodes of binge eating, characterized by both of:
- eating more food than a normal person would eat in a given time period ex. 2 hrs
- sense of lack of control
2) recurrent inappropriate compensatory behaviors to prevent weight gain
3) on average, occurs ate least once a week for three months
4) self-evaluation unduly influenced by body shape and weight
5) disturbance does not occur exclusively during episodes of AN

433
Q

AN vs BN

A
  • body weight: AN < BN
  • restriction more prevalent in AN
  • purging in AN is for weight loss, not as compensation
  • in BN, purging and binging coupled more closely in time + no weight loss typically
434
Q

EDNOS examples

A

1) atypical AN: all criteria met except weight normal
2) BN or BED with low frequency or limited duration
3) purging disorder: no binging
4) night eating syndrome: binging at specific times at night

435
Q

assessment and diagnostic considerations in eating disorders

A
  • rule out medical conditions: ex. Kleine-Levin symptom, GI problems, HIV
  • rule out other mental disorders: MDD, phobias
  • can only have on ED at a time
436
Q

criticisms of pre DSM-5 ED diagnosis

A
  • ED should be rated as one disorder on a continuum of severity (research suggests)
  • 50% people who have AN will also develop BN or other bulimic problems at some point in their life
  • people often switch from one category to another and back (decreases utility of diagnosis)
  • most AN in teens, BN in late teens-early adulthood, BED in adults –> dimension of age might be involved as well
437
Q

alternative models for ED

A

1) age
2) weight
3) anxiety seems more related to AN, depression to BN/BED
4) distinct physiological consequences

438
Q

incidence and prevalence of ED

A
  • some research suggesting in creasing prevalence
  • could be due to more awareness or changes to DSM-5
  • most common in teen women
439
Q

ED prognosis

A
  • highest mortality rate (starvation, dehydration and nutritional complications
  • variable treatment response: only 50% able to stop binging/purging, high relapse rates, commonly requires in and outpatient treatment
  • people might switch diagnoses after recovering from one
  • treatment can be too late or lethal if corrected too quickly (refeeding syndrome)
440
Q

consequences of ED

A
  • significant physical and psychological consequences
  • most are reversible over time
441
Q

lanugo

A
  • peach fuzz to maintain warmth
442
Q

Russell’s sign

A
  • patterns of scars/signs on knuckles resulting from purges
443
Q

genetic etiology of EDs

A
  • predisposition may be genetic
  • possible link to reduced density of serotonin transporters
  • gender differences in serotonergic system may make women more susceptible (dysregulated serotonin more likely, dieting alters brain serotonin more significantly in women compared to men)
444
Q

sociocultural factors in ED

A
  • thin ideals increased dramatically, even though body weight has increased over time –> discrepancy leads to negative affect (guilt/shame), body dissatisfaction, dieting, exercise
  • internalization of media images is risk factor, fueled by social media
  • for men: ideal is to become more muscular
445
Q

are EDs culturally-bound?

A
  • AN/BN occur more frequently in westernized culture
  • AN does not appear to be culturally bound
  • however, weight concerns and BN may be
  • culture-bound = syndrome restricted to a limited number of cultures by reason of certain of their psychosocial features
446
Q

family factors in ED

A
  • family communication about weight, food, thinness and dieting can be risk factor
  • ex. mothers who diet or who are dissatisfied with weight/appearance are more likely to have daughters that are similar
  • critical, coercive, emphasize weight/appearance = worse outcomes for ED
  • ex. daughters with ED rated less attractive by mothers, perceived lack of care from them
  • ex. children with mothers with ED have higher concerns about weight, shape and diets (also higher negative affect)
447
Q

personality/individual differences in ED

A

1) AN/BN: perfectionism, obsessiveness, compliance, lack of awareness of feelings/emotions (alexithymia), negative self view
2) BN: impulsivity
3) other IDs: low self-esteem, identity disturbance, depressive affect, poor body image, dieting, excessive exercise
*some research suggests BPD/OCPD symptoms in EDs

448
Q

maturational factors in ED

A
  • puberty takes females farther away from ideal weight + different levels of body fat
  • puberty also increases their awareness of sex roles, consent, dating, sexuality, negative portrayal of overly sexual women in media –> more stressful for females
449
Q

adverse events in ED

A
  • traumatic events affect self-esteem, body image and sense of control
  • high rates of sexual trauma or abuse in EDs
  • some studies suggest trauma is more strongly associated with bulimic behavior as opposed to restriction
450
Q

integrative models for EDs

A
  • integrate many of the risk factors and other models
451
Q

ED in males?

A
  • lower prevalence
  • men exposed to less diet-related info
  • men tend to want to increase weight (muscle mass)
  • some evidence that EDs are higher in LGBTQ+ individuals, but body dissatisfaction is a more prominent predictor
452
Q

biological approaches to treating EDs

A
  • AN: SSRIs may exacerbate eating symptoms (side effect = decreased appetite), so best treatment is to increase weight through food (safe and gradual) and develop normalized eating patterns (ex. by group meals)
  • BN/BED: SSRIs can improve, but CBT is better
453
Q

CBT for EDs

A
  • three stages:
    1) establish regular pattern of eating: psychoeducation, models of EDs and connection between restriction/binges, self-monitoring, food diaries
    2) normalized eating without dieting: behavioural strategies for meal planning, stimulus control, problem-solving to reduce stressors/negative affect, modifying dysfunctional thoughts and beliefs (especially about weight/shape)
    3) strategies to maintain change and prevent relapse, ex. mindfulness
454
Q

other ED therapies

A

1) IPT: maladaptive personal relationships and ways of interacting with each other (doesn’t actually target eating behaviour!)
2) nutritional therapy and meal support
3) family therapy: explore whole family dynamic and gives responsibility for recovery to patient and relatives

455
Q

prevention interventions for EDs

A
  • self-help and internet-based protocols about eating
  • campaigns/school programs to reduce dissatisfaction with body image, especially among girls
456
Q

history of addiction

A

1) pre-industrial = morally responsible
2) WWII = moral/disease
3) late 90s = brain disease model of addiction (BDMA) = biological
4) current = debate about brain disease

457
Q

current definitions of addiction

A

1) disease/BDMA
2) moral
3) psychological: personal deficiencies (sensitivities)
4) learning
5) spiritual
6) nature: innate drive
7) sociological: environmental deficiencies, ex. SES
8) disorder-of-choice
9) biopsychosocial

458
Q

categories of substance use disorders

A

1) substance use:
- alcohol
- cannabis
- PCP/other hallucinogen
- inhalant
- opioid
- sedative/hypnotic/anxiolytic
- stimulant
- tobacco
- other/unspecified
2) behavioural use:
- problem gambling
- internet gaming
3) absent:
- caffeine use
- polysubstance use

459
Q

why was addiction reintroduced into DSM-V?

A
  • know that a number of behaviors can also be addictive
460
Q

substance abuse vs dependence in DSM IV

A
  • abuse = 1 of 4 abuse symptoms (relatively less severe)
  • dependence = 3 of 7 dependence symptoms (would trump abuse)
461
Q

diagnostic indicators of substance abuse

A

1) impairment of control
2) social impairment
3) risky use
4) pharmacological dependence (tolerance and withdrawal)

462
Q

tolerance

A

need increased amounts to achieve same effect

463
Q

withdrawal

A
  • unpleasant and sometimes dangerous symptoms when substance is removed from body
  • ex. nausea, headache, tremors
  • result of changes that body has undergone in order to adapt to continued presence of drug
464
Q

substance-induced disorders

A

symptoms only occur during substance use

465
Q

impairment of control (1-4)

A

1) substance taken in larger amounts or over longer period than intended
2) persistent desire or unsuccessful attempts to cut down or control use
3) great deal of time is spent obtaining, using or recovering from substance
4) craving or strong desire/urge to use (that controls behavior)

466
Q

social impairment (5-7)

A

5) recurrent use resulting in failure to fulfill major obligations at work, school or home
6) continued use despite persistent/recurrent social or interpersonal problems caused by substance effects
7) important social, occupational or recreational activities are given up or reduced because of substance use

467
Q

risky use indicators (8-9)

A

8) recurrent use in situations where it is physically dangerous
9) use despite knowledge of persistent or recurrent effect on physical or psychological problems

468
Q

pharmacological dependence (10-11)

A

10) tolerance to the substance
11) withdrawal syndrome

469
Q

alcohol withdrawal and reinforcement

A
  • negative reinforcement: drinking again reduces withdrawal
470
Q

alcohol withdrawal length

A
  • can last up to 1 year
471
Q

alcohol/substance use disorder DSM criteria

A

1) problematic pattern of usage leading to clinically significant impairment or distress, must have 2+ of symptoms within a 12 month period

472
Q

SUD severity

A
  • based on symptom count
  • mild = 2-3
  • moderate = 4-5
  • severe = 6+
473
Q

other substance use disorders

A

1) substance intoxication: lasts only for time intoxicated
2) substance withdrawal
3) substance or medication-induced [category] disorder (ex. cannabis-induced psychotic disorder)

474
Q

polysubstance abuse

A
  • no longer disorder in DSM
  • when 2+ substances are misused simultaneously
  • fairly common among SUD patients
475
Q

alcohol use trends

A
  • many cultures have underlying social acceptability to drink and be drunk
  • use peaks in mid-twenties, higher among single, high-income and post-secondary education
  • however, the heaviest drinkers are low education and out of work
476
Q

alcohol use categories

A

1) light infrequent: low # and frequency
2) light frequent: low #, high frequency
3) heavy infrequent: high #, low frequency
4) heavy frequent: high # and frequency (riskiest group)

477
Q

AUDIT

A

popular screening scale (free) for risk of AUD –> relationship between consumption levels and overall risk for AUD

478
Q

binge drinking

A

5+ drinks in one sitting

479
Q

updated government of Canada guidelines for alcohol use

A
  • no risk = 0 drinks per week
  • any amount of drinks increases risk of harm (cumulatively)
  • body weight not considered here or in DSM!
480
Q

how does alcohol work?

A
  • active ingredient = ethyl alcohol
  • effects: anxiety reduction, euphoria, sense of well-being, reduced inhibitions
  • passes into blood from stomach, most absorbed by small intestine
  • rate and peak level of absorption depend on how quickly alcohol gets through stomach and intestine
  • concentration expressed in blood alcohol level (BAL)
481
Q

blackouts from alcohol use

A
  • drinking quickly and on empty stomach
  • person cannot recall key details or entire events
482
Q

short-term effects of alcohol

A

hangovers, sleep disruption, DUI, impulsive behaviors

483
Q

social effects of alcohol

A
  • can affect relationships and social life physical ,health, happiness, finances, homelife/marriage, work/school, legal problems
484
Q

fetal alcohol spectrum disorder

A
  • mothers drinking during pregnancy associated with physical abnormalities and cognitive deficits
  • fetal alcohol syndrome is the most severe form
485
Q

(Wernicke-)Korsakoff’s syndrome

A
  • serious cases of alcohol use
  • cell loss in hypothalamus, thalamus and hippocampus
  • impaired memory/loss of contact with reality
  • aka “Wet Brain”
486
Q

biological/genetic etiology of AUD

A
  • enzyme levels: aldehyde dehydrogenase (metabolizes alcohol) reduced in Asian-descent individuals
  • physiological sensitivity to rewarding properties of alcohol
  • neurotransmitters: GABA, serotonin, beta-endorphin
  • genes: GABA, glutamate, serotonin, dopamine, cholinergic, opioid systems
  • MZ > DZ twin concordance rate, stronger for males
  • males at higher risk generally
487
Q

psychological factors in AUD

A
  • “addictive personality”: behavioral disinhibition, negative emotionality, neuroticism
  • theories:
    1) tension-reduction hypothesis: negative reinforcement
    2) alcohol expectancy theory: alcohol-related cognitive beliefs
    3) classical conditioning and behavioral tolerance (feel more functional even when intoxicated)
488
Q

sociocultural factors in AUD

A
  • rite of passage, sign of maturity, cultural or family tradition, attitudes
  • adolescent drinking typically mirrors parent patterns (ex. coping with stress)
489
Q

sedatives, hypnotics, anxiolytics (barbs/benzos)

A
  • CNS depressants
  • barbituric acid first treatment of anxiety and tension –> parent compound of barbiturate drugs, high addiction potential
  • benzodiazapenes are new class of drugs, but still have moderate potential for addiction (esp because of neg. reinforcment)
  • dangerous when combined with other depressants (ex. alcohol) because of synergistic effects (can cause death)
490
Q

effects of barbs/benzos

A
  • small doses = mild euphoria
  • larger doses = slurred speech, poor coordination, impairment of judgment and concentration, sleep
  • chronic use: depression, fatigue, mood swings, paranoia, memory/judgement impairment
491
Q

abstinence syndrome

A
  • caused by benzodiazepine withdrawal
  • insomnia, headaches, aching, anxiety, depression
  • can last for months
  • in serious cases, abrupt discontinuation can cause delirium, convulsions, death
492
Q

tobacco (nicotine)

A
  • small but potent dose of nicotine in cigarettes
  • fast acting because enters through inhalation, transported quickly to brain
  • many long-term health risks, even with second-hand smoke
493
Q

nicotine effects

A
  • pure: interferes with thinking and problem solving, agitation and irritability, mood changes
  • cigarettes: increases alertness, improves mood = positive reinforcement
494
Q

tobacco dependence

A
  • considered highly addictive
  • most addiction is to prevent withdrawal (negative reinforcement)
  • lots of time spent obtaining cigarettes, most people recognize health consequences but continue regardless
  • some people might be more sensitive to nicotine (related to effect on dopaminergic neurons)
495
Q

tobacco and alcohol effect

A
  • synergistic
  • alcohol stimulates dopamine release indirectly at cell body and terminals
  • nicotine mimics Ach at nicotinic receptors to directly activate dopamine cells
496
Q

amphetamines

A
  • mimic adrenaline
  • originally for medical purposes: asthma, ADHD, narcolepsy, suppressing appetite for obesity
  • two forms: methamphetamine and dextroamphetamine (legally prescribed)
497
Q

amphetamine effects

A
  • low dose: increase alertness, focus attention, improved performance on cog. tasks (popular for truckers, athletes and students)
  • high: exhilaration, extroversion, confidence
  • very high: agitation and anxiety
  • chronic: hallucinations, delirium, paranoia (toxic psychosis)
  • physical: increased/irregular heartbeat, fluctuations in BP, hot/cold flashes, nausea, weakness, dilation, weight loss, seizures, confusion, coma
  • potential for violent and aggressive behavior while on drug
498
Q

amphetamine tolerance, dependence and withdrawal

A
  • ecstasy: debate over whether there is a permanent depletion of serotonin in the long term
  • amphetamine tolerance and dependence: quick because of crashing (fatigue, irritability, sadness, cravings)
  • withdrawal: apathy and prolonged sleeping
499
Q

cocaine effects

A
  • low dose: euphoria, confidence, alert, talkative, reduced appetite, increased excitement and energy
  • high: poor muscle control, confusion, anxiety, anger, mood swings, aggression, anhedonia, weight loss, insomnia, toxic psychosis
  • physical: increased blood pressure and temperature, irregular heartbeat, chest pain, nausea, blurred vision, fever, muscle spasms, convulsions, coma, death
500
Q

cocaine

A
  • used to reduce fatigue and induce euphoria (triggers dopamine release)
  • originally in many drinks, cigarettes, used occasionally as local anesthetic
  • snorting increases metabolism rate
  • short-acting, wears off quicky
501
Q

cocaine dependence and withdrawal

A
  • huge crash: intense cravings, depression, paranoia, fatigue
  • can take more than a month to get rid of withdrawal
502
Q

caffeine

A
  • also a stimulant
  • dopamine, serotonin and NE
503
Q

caffeine effects

A
  • 1-2 doses: increase attention, problem-solving skills, improves mood
  • 6-7 doses: muscle tremors, agitation, excessive talkativeness, disorganized thinking, rapid/irregular heartbeat (resembles hypomania)
504
Q

caffeine dependence

A
  • > 350mg used per day
  • leads to unpleasant withdrawal symptoms
505
Q

opioid types

A

1) morphine (severe pain)/codeine (small doses in cough syrups and painkillers): refined from opium
2) semi-synthetic: derived from natural opiates
3) synthetic forms: manufactured
4) endogenous form in humans: endorphins

506
Q

opioid function

A

CNS depressant

507
Q

prescription opioid abuse

A
  • major problem in Canada
508
Q

opioid effects

A
  • mimic endorphins, affecting brain and spinal cord
  • low doses: euphoria, relaxation, appetite suppressant, restlessness, nausea and vomiting
  • high: dangerous, constricted pupils, blue/cold skin, slow breathing, coma, respiratory depression
  • chronic: respiratory and pulmonary problems, endocarditis, abscesses, liver disease, brain damage, HIV (needles)
509
Q

opioid overdoses

A
  • easy because of tolerance (especially behavioral body tolerance)
510
Q

opioid dependency

A
  • severe withdrawal symptoms, begin ~8hrs
  • 36hrs: muscle twitching, cramps, hot flashes, HR/BP fluctuations, sleeplessness, vomiting, diarrhea
  • can last for 10 days
  • milder opiates often used to cope
511
Q

cannabis effects

A
  • depressant (lowered inhibitions) and stimulant (increased HR)
  • low: mild changes in perception, enhancement of physical experiences, mildly euphoric, sociability, well-being, relaxation (some have bad reactions)
  • large doses can produce hallucinations, problems with complex motor skills, short-term memory, reaction-time and attention
  • long-term: lung problems, cancer risk, psychosis risk
  • chronic problem: amotivational syndrome
512
Q

cannabis tolerance and withdrawal

A
  • milder withdrawal effects
  • irritability, anxiety, loss of appetite, restlessness, sleep disturbances, anger/aggression
513
Q

amotivational syndrome

A
  • apathy, detachment and abandonment of school/work
  • brain function altered by chronic cannabis use
  • may also be related to depression
514
Q

marijuana therapeutic effects

A
  • low doses alleviate nausea, encourage eating and relieves pressure in eyes
  • THC is main active ingredient, binds to endogenous endocannabinoid receptors
515
Q

hallucinogens

A
  • change person’s mental state by inducing perceptual and sensory distortions
  • many ways to ingest
  • effects are fast and short-acting
516
Q

hallucinogen effects

A
  • subjective effects: depending on expectations, personality, setting (ex. uncomfortable or unsafe may lead to intense fear/anxiety that can escalate into panic/psychotic episodes)
  • sensory experiences: vivid visual hallucinations, perceptual distortions, synesthesia
  • physiological effect: excites CNS, mimics manic episode, increases 5HT in brain, dilated pupils, increased HR/BP, increased alertness
  • risk of injury comes from experience on drug
517
Q

problem gambling prevalence

A
  • higher risk for males and being indigenous
518
Q

problem gaming interventions

A
  • focus on motivation for change
  • internet-based CBT has preliminary efficacy for reducing problem gaming
519
Q

gambling disorder DSM criteria

A

1) persistent and recurrent problematic gambling, impairment/distress, 4+ of the following in 12-month period:
- needs to gamble with increasing amounts of money for desired excitement
- restless/irritable when attempting to cut down or stop
- repeated unsuccessful efforts to control gambling
- often preoccupied with gambling
- often gambles when feeling distressed
- after losing money, returns to get even
- lies to conceal extent of gambling
- has jeopardized or lost a significant relationship, job, educational or career opportunity
- relies on others for money to relieve financial situations caused by gambling
2) not better explained by mania

520
Q

internet gaming disorder criticism

A
  • internet = tries to acknowledge interpersonal aspect, but leaves out other video games
521
Q

internet gaming disorder prevalence

A
  • risk for adolescent males
522
Q

internet gaming disorder DSM

A

1) 5+ within 12 months:
- preoccupation with internet games
- withdrawal symptoms
- tolerance
- unsuccessful attempts to control participation
- loss of interest in other activities
- excessive use despite knowledge of psychosocial problems
- deceived family members/therapists, etc.
- use to escape
- lost significant relationship, job or educational/career opportunity

523
Q

SUD routine treatment

A
  • inpatient program focusing on biological dependence (withdrawal)
  • person allowed to detoxify under medical supervision, sometimes includes prescriptions to wean off drugs
  • then, psychological dependence treatment: education, individual counselling, group therapy for social skills and communication
  • abstinence is generally the goal, but harm reduction or moderation may be more optimal/realistic
524
Q

AUD pharmacotherapy

A
  • benzodiazepines
  • GABA antagonist to reduce cravings
  • GABA agonist to reduce withdrawal
  • inhibitors of alcohol dehydrogenase = more negative effects of alcohol
525
Q

alcoholics/narcotics anonymous

A
  • addiction seen as a disease
  • goal is complete abstinence
  • focus on person as powerless and need for religion or higher power
526
Q

SMART recovery programs

A
  • secular, flexible and empirically supported
  • focus on skill building
  • goal can be either abstinence or harm reduction
527
Q

behavior therapy for SUD

A
  • increase awareness of cues and associated influences
  • aversive conditioning
  • contingency management: rules for rewards and punishments for small steps
  • practices behavioral coping and how to develop contingency contracts
528
Q

cognitive/behavioral self-management for SUD

A
  • restructuring thoughts about drinking (utility, meaning)
  • recognizing and being aware of patterns
  • monitoring and SMART goals
529
Q

relapse prevention in SUD

A
  • post-treatment
  • relapse seen as inadequate cognitive and behavioral coping skills
  • help individuals recognized distorted self-defeating thoughts and learn from relapse (cognitive restructuring around guilt/failure)
  • build resilience
530
Q

marital/family therapy for SUD

A
  • focus on relationship
  • patterns of interaction can maintain substance use behaviors (ex. codependence)
531
Q

brief interventions for SUD

A
  • designed to explore concerns about changing (ex. pros/cons)
  • motivational interviewing to seek and encourage readiness for change
532
Q

stages of motivation for change

A

1) precontemplation: denial of consequences, not considering change
2) contemplation: ambivalence, some hesitations
3) preparation: decided to make change
4) action
5) maintenance
(6) relapse)

533
Q

treatment for nicotine use disorder

A
  • psychological: counseling, online or community support groups, self-help materials (mostly behavioral or cognitive)
  • some support for hypnosis
  • nicotine replacement products: reduce cravings and withdrawal, breaks behavioral habits between smoking and environment
  • some medications
534
Q

cocaine use treatment

A
  • similar therapy to general SUD
  • some medication to combat short-term withdrawal
535
Q

opioid biological treatment

A
  • naltrexone: opioid antagonist that interferes with binding
  • methadone: heroin replacement to reduce cravings after withdrawal
  • these biological interventions work best with other adjunct programs
536
Q

harm-reduction techniques

A
  • don’t reduce use frequency
  • safe injection sites, often coupled with counseling
  • needle exchange programs (reduce risk of HIV and hepatitis C)
537
Q

non-abstinent support groups

A
  • abstinence achieved in very low percentage of people who attend abstinent-goal programs
538
Q

traits vs states

A
  • traits = consistent across situations, persistent
  • states = temporary, conditional or transient patterns
539
Q

personality disorder general definition

A
  • maladaptive patterns of personality traits
  • enduring pattern of inner experience and behavior that deviates from normal range
  • pervasive, rigid and inflexible across situations and people
  • onset = adolescence or early adulthood
  • stable over time, leading to distress/impairment, including in other people
  • restricted range of traits compared to those without PDs
540
Q

six formal criteria for defining PDs

A

1) pattern of behavior manifested in at least two of: cognition, emotion, interpersonal functioning or impulse control
2) enduring pattern of behavior, rigid and consistent across a broad range of personal and social situations
3) behavior should lead to significant distress in social, occupational or other important areas of functioning ex. relationships
4) stability and long duration of symptoms with onset in adolescence or earlier
5) behavior cannot be accounted for by another mental disorder
6) behavioral patterns not the result of substance or medical condition

541
Q

egosyntonic vs egodystonic

A
  • syntonic = not viewed as problematic or impairing, instead consistent with one’s self-image/goals
  • dystonic = cause distress and are viewed as problematic, in conflict with who they are or want to be
542
Q

clusters of PDs

A

1) odd and eccentric: paranoid, schizoid, schizotypal
2) dramatic, emotional or erratic: antisocial, borderline, histrionic, narcissistic (highly heterogenous cluster, may be underreported)
3) anxious and fearful: avoidant, dependent, obsessive-compulsive (may be overrepresented by self-report questionnaires)

543
Q

previous PDs now removed from DSM

A
  • depressive personality
  • passive-aggressive (negativistic)
  • sadistic
  • self-defeating (masochistic)
544
Q

why is consideration of PD important?

A
  • could disrupt alliance between therapist and client
  • can be mistaken for Axis I condition and/or can worsen Axis I condition
  • prognosis is somewhat poor (although improving)
545
Q

PD prevalence rates

A
  • difficult to determine
  • high in outpatient samples, even higher in inpatient
  • very high in prisons (largely because of ASPD)
  • some gender disparities: females = avoidant, dependent, paranoid, borderline; males = antisocial)
546
Q

paranoid personality disorder

A
  • pervasive distrust and suspiciousness of others, such that their motives are interpreted as malevolent
  • beginning in early adulthood
  • present in a variety of contexts
  • 4+ symptoms
547
Q

schizoid personality disorder

A
  • pervasive pattern of detachment from social relationships
  • restricted range of expression of emotions in interpersonal settings
  • beginning by early adulthood
  • present in variety of contexts
  • 4+ symptoms
548
Q

schizotypal personality disorder

A
  • pervasive social/interpersonal deficits
  • acute discomfort with and reduced capacity for close relationships
  • cognitive or perceptual distortions (but not to the degree of delusions or hallucinations)
  • eccentricities of behavior
  • beginning early adulthood
  • present in variety of contexts
  • 5+ symptoms
549
Q

schizotypal vs psychotic disorder

A
  • some overlap
  • difference is severity and quality of symptoms
550
Q

histrionic personality disorder

A
  • pervasive pattern of excessive emotionality and attention seeking
  • beginning by early adulthood
  • variety of contexts
  • 5+ of the following
551
Q

narcissitic personality disorder

A
  • pervasive pattern of grandiosity (in fantasy or behavior)
  • need for admiration
  • lack of empathy
  • beginning by early adulthood
  • variety of contexts
  • 5+ of the following
552
Q

avoidant personality disorder

A
  • pervasive pattern of social inhibition
  • feelings of inadequacy
  • hypersensitivity to negative evaluation
  • beginning by early adulthood
  • variety of contexts
  • 4+ of the following
553
Q

dependent personality disorder

A
  • pervasive and excessive need to be taken care of
  • leads to submissive and clinging behavior
  • fears of separation
  • beginning by early adulthood
  • variety of contexts
  • 5+ of the following
554
Q

obsessive-compulsive personality disorder

A
  • pervasive pattern of preoccupation with orderliness, perfectionism and mental and interpersonal control
  • comes at the expense of flexibility, openness, and efficiency
  • beginning by early adulthood
  • variety of contexts
  • 4+ of the following
555
Q

issues with treatment for PDs

A
  • most patients are not upset by symptoms and do not seek treatment, high dropout rates
  • comorbid PDs worsens prognosis of Axis I conditions
  • challenge for the therapist given relationship difficulties
  • barriers: lack of training, complexity of disorder
556
Q

how to improve treatment for PDs

A
  • conceptualize PD as both biological and psychological
  • assess the individual’s amenability to treatment (how likely they are to stay in)
  • effective treatment is flexible and tailored
  • goal is to improve personality-style functioning: flexibility and adaptability
557
Q

pharmacological treatments for PDs

A
  • no first line options: antidepressants, anxiolytics and antipsychotics are common
  • ASPD/BPD: combo of medications
  • schizotypal PD: typical antipsychotic and antidepressants
558
Q

object-relations therapy for PD

A
  • differentiation of self from close others (individuation)
  • relationship between client and therapist helps supportively confront patients defenses and distortions
  • long-term, usually 1+ years
559
Q

CBT for PDs

A
  • cognitive restructuring of core beliefs
  • examining flexibility of beliefs
  • behavioral experiments
  • similar to schema therapy and transference-focused therapy
560
Q

psychopathy

A
  • broader constellation of symptoms related to emotional, interpersonal, behavioral features rooted in inability to experience empathy and remorse
  • often more criminality and selectively impulsive compared to ASPD (which is more aggression/impulsivity)
  • usually target people who are easy to manipulate
561
Q

ASPD DSM criteria

A

1) pervasive pattern of disregard for and violation of the rights of others, occurring since 15, 3+ of:
- failure to conform to social norms regarding lawful behaviors, indicated by repeatedly performing acts that are grounds for arrest
- deceitfulness for personal profit or pleasure: repeated lying, use of aliases, conning others
- impulsivity or failure to plan ahead
- irritability and aggressiveness: repeated physical fights or assaults
- reckless disregard for safety of self or others
- consistent irresponsibility: failure to sustain consistent work behavior or honor financial obligations
- lack of remorse: being indifferent to or rationalizing having hurt, mistreated or stolen from another
2) 18+
3) evidence of CD before 15+ (does not have to be diagnosed)
4) rule out psychotic disorders

562
Q

ASPD etiology

A

1) family systems: parenting behaviors
2) genetics: aggressive and impulsive markers with high heritability
3) environment: “criminogenic” = poor parenting, neglect, abuse
4) fearless hypothesis: higher threshold for fear
5) emotional/physical abuse: punishment not contingent with behavior leads to indifference from physical punishment or being oppositional to attempts at controlling them

563
Q

ASPD treatment

A
  • burnout tends to happen around 40s
  • usually delivered in forensic hospitals or prisons
  • structured programmatic materials for psychoeducation, beliefs about aggression/antisocial attitudes, developing self-regulation, assertiveness, substance use, problem-solving
  • short-term use of psychotropic medications sometimes helps
564
Q

responsivity factor in ASPD

A
  • treatment works better when matched to a patient’s needs and interpersonal style
565
Q

machiavellianism

A

callous, manipulative, amoral and deceptive behavior to achieve power in politics and society

566
Q

psychopathy etiology

A
  • insensitivity to emotional content of information = abnormal PFC, hippocampus, basal ganglia, amygdala
  • different means of processing emotional material to compensate for absence of appropriate limbic input
  • lower serotonin and increased dopamine
  • moderate levels of heritability
  • association with early emotional deprivation
567
Q

psychopathy prognosis

A
  • typically lifelong
  • precursors include callous/unemotional traits seen in childhood CD/ODD
568
Q

“borderline” term

A
  • border between neurosis and psychosis
  • new term suggested is pervasive emotion dysregulation disorder –> this is the core feature
  • suggested to be more of an emotional disorder vs PD
569
Q

common dimensions in BPD

A

1) affective instability and dysregulation (most common)
2) identity disturbance / disturbed sense of self
3) interpersonal hypersensitivity
4) behavioral dyscontrol (impulsivity)

570
Q

psychotic features in BPD?

A
  • none
  • perceptual disturbances and strong beliefs can occur, but more consistent with dissociation
571
Q

BPD prevalence

A
  • more common in women
  • after ~1- years, about half no longer have pattern of behavior that meets full BPD criteria
572
Q

BPD DSM criteria

A

1) pervasive pattern of instability of interpersonal relationships, self-image and affects and marked impulsivity beginning early adulthood, present in variety of contexts, 5+ of:
- frantic efforts to avoid real or imagined abandonment
- pattern of unstable and intense interpersonal relationships: alternating between extremes of idealization and devaluation (“splitting”)
- identity disturbance
- impulsivity in at least two areas that are potentially self-damaging
- recurrent suicidal behavior, gestures, threats, or self-mutilation
- affective instability due to marked reactivity of mood
- chronic feelings of emptiness
- inappropriate, intense anger or difficulty controlling anger
- transient, stress-related paranoid ideation or sever dissociative symptoms

573
Q

BPD vs BP-II

A
  • quick shifts in BPD (~few hours), almost never lasts a day
574
Q

diagnostic comorbidity of BPD

A
  • high
  • suggests complex emotional disorder
575
Q

emotion dysregulation in BPD

A
  • under normative conditions, inability to change in a desired way: emotional cues, experiences, actions, verbal responses, nonverbal expressions
  • seen as consequences of inability to cope effectively in cognitive way –> high utilization of psychiatric services
576
Q

development of emotion dysregulation in BPD

A
  • diathesis-stress model
    1) biological/temperament = emotionally sensitive
    2) psychological/social = invalidating environments that exacerbate biological vulnerability, shaping thoughts about emotion/expression and limiting opportunities to learn appropriate regulation
577
Q

DBT rationale

A
  • CBT was difficult because pushing people to change without acceptance is difficult
  • shows promise for multiple conditions in decreasing emotion dysregulation
578
Q

DBT foundations

A

1) Rogerian: provide source of validation and nonjudgmental support
2) learning theory: behavior patterns become established through classical learning mechanisms
3) zen buddhism: suffering results from particular attachment to things, nonjudgmental acceptance of reality reduces this
4) CBT: change is required and necessary to feel better, focus on skills-based learning, exercises and activities

579
Q

DBT general overview

A
  • individual and group sessions each week
  • 6 months to a year
  • telephone consult in crisis times (problem-solving coaching)
  • team consultation meetings for therapists
  • ancillary treatments (pharmacotherapy, inpatient, day treatment, etc.)
580
Q

DBT goal hierarchy

A

1) reduce suicidal behavior
2) reduce therapy interfering behavior
3) reduce behaviors that interfere with quality of life
4) increase behavioral and emotion regulation skills
5) decrease post-traumatic stress behaviors
6) increase self-respect behaviors

581
Q

DBT main principle

A
  • dialectic: process of achieving balance between two opposing processes
  • pushing hard for change vs. acceptance of problems as they are
  • communication is needed for balance
582
Q

core strategies of DBT

A

1) validation
2) commitment
3) behavioral chain analysis
4) problem-solving

583
Q

validation in DBT

A
  • communicating that something about the client’s behavior makes sense or is understandable within the current context
584
Q

commitment in DBT

A
  • getting patients to commit to change (clear)
  • explore pros and cons
  • Devil’s advocate
  • foot in the door, door in the face
  • connect to prior commitments
  • freedom to choose
  • generate hope and/or cheerlead
585
Q

behavioral chain analysis in DBT

A
  • make patients more aware of their emotions, thoughts, feelings and behaviors
    1) identify behavior
    2) identify vulnerabilities
    3) identify prompting events
    4) identify links between prompting event and behavior
    5) identify consequences
586
Q

problem-solving in DBT

A
  • after behavioral chain analysis
  • implement to avoid recurrence of the behavior
  • increase environmental safety or teach distress tolerance skills
587
Q

PD diagnostic issues (related to etiology and treatment efficacy)

A
  • are they disorders or just traits?
  • difficulty in defining disorders that is unbiased, reliable and leads to effective treatment/predictions
588
Q

gender/cultural issues with PD diagnosis

A
  • potential confounds
  • ex. spirit beliefs may be schizotypal, but can also be cultural
  • ex. emotional PD diagnosed more often in Hispanic individuals (show emotions more)
  • ex. schizotypal more often diagnosed in African-Americans
  • sex stereotypes: histronic for women, hesitant to diagnosis males as histronic or females as antisocial
589
Q

reliability of PD diagnosis

A
  • poor across clinicians and measures used
  • requires thorough evaluation, therefore not always completed
  • some conditions may not be as chronic as once believed
590
Q

comorbidity and diagnostic criteria overlap in PD

A
  • similar symptoms in one or more PDs when they should be distinct
  • some vague criteria
  • highly comorbid with Axis 1 conditions
591
Q

proposed dimensional model for PD

A
  • deleting dependent, histronic, paranoid and schizoid
  • because of symptom overlap and biases
  • already absent from ICD
592
Q

attachment theory etiology of PD

A
  • children learn to relate to others by the way their parents relate to them
  • positive = skills and confidence to relate effectively with others
  • negative = lack confidence in relationships
593
Q

cognitive-behavioral etiology of PDs

A
  • schemas and compensatory strategies to prevent belief from being activated
  • coping manners may have been adaptive in childhood, but no longer are in adulthood
  • parents may model inappropriate styles or unintentionally reinforce the opposite of the desired behavior
594
Q

biological etiology of PDs

A
  • strongest evidence for antisocial PD
  • some dimensions: cognitive-perceptual organization, impulsivity/aggression spectrum, affective stability-instability, anxiety-inhibition
  • transmission of non-disorder specific genetic risk factors (relatives of disordered individual sometimes have PDs)
595
Q

course takeaways

A

1) dividing line between normal and abnormal is unclear
2) DSM is still just a guideline
3) the essential ingredients of therapy are not unique to therapy