Module 3: Part 4 Flashcards

1
Q

What is fetal programming?

A
  • In utero environment influences the development of the fetus and can have long-lasting effects on the child - Fetal programming sets the trajectory BUT can be influenced later in vivo (e.g. reversible)
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2
Q

What is the Barker hypothesis?

A
  • CHD, T2DM, Stroke and HTN originate in utero in response to undernutrition during fetal life
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3
Q

What are the risk factors according to Barker hypothesis?

A
  • In vivo (Obesity, Smoking) | In utero (Low Birth Weight —> Increased risk of CHD/HTN) - N.B. undernutrition = LBW in this context
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4
Q

What increases and decreases the risk of LBW?

A
  • If genetically determined to be small —> no increased risk - If babies grow less than genetically destined —> Increased risk - Those that grow less than genetically destined have catch-up growth (accelerated weight gain) during childhood
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5
Q

What is the Fetal Origin of Adult Disease?

A
  • Birth weight, Birth phenotype (size), Early postnatal growth —> Increased risk of Adult life
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6
Q

What is the most common complication of Pregnancy?

A
  • Depression (10%) - Maternal depression is often missed - Maternal anxiety and depression associated with Maternal Adverse Childhood Experience (e.g. sexual abuse)
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7
Q

What is Maternal anxiety associated with?

A
  • Fetal heart rate
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8
Q

What are examples of Maternal Prenatal Stress associated with Development?

A
  • Maternal anxiety and depression - Maternal daily hassles - Anxiety relating to Pregnancy - Family discord - Child has increased risk of anxiety, depression, ADHD, CD, Autism/autism spectrum symptoms
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9
Q

What are causes of antenatal maternal anxiety/depression?

A
  • Early childhood trauma-adverse childhood experiences (ACES) - Maternal history of sexual abuse predicts elevated anxiety/depression from pregnancy to 33 months
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10
Q

Describe prenatal stress more common in low and middle income countries

A
  • Symptoms of perinatal depression and anxiety (roughly 25% compared with roughly 15%) - Pregnancy specific anxiety (can be high levels of maternal and infant death - Interpersonal violence (in Afghanistan 92% of women thought wife beating justified) - Effects of natural disasters e.g. Nepal earthquake - War and other conflicts - Refugees
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11
Q

What is prenatal stress also associated with?

A

Increased risk of - Reduced birthweight and gestational age - Mixed handedness - Altered finger print pattern - Decreased telomere length (may be associated with decreased life expectancy - Altered microbiome - Asthma - Altered immune function

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12
Q

How is pregnancy related anxiety associated with microbiome pattern in newborn meconium

A
  • Less varied pattern of different types of microbiome if the mother was more anxious
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13
Q

Describe animal studies of relationship between pre-natal mood and child neurodevelopment

A
  • Role of HPA axis and cortisol | Prenatal stress affects neurodevelopment of offspring - Stress pregnant animal + follow outcomes in child (cross-fostered by control rat just given birth to reduce post-natal rearing effects) - Offspring of stressed mothers appear more anxious (Increased cortisol response to novel stressor compared with control)
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14
Q

What is the ALSPAC study?

A
  • Avon Longitudinal Study of Parents and Children - Overall top 15% most anxious/depressed mothers have 2x increased rate of child’s probable mental disorder at age 13 - Prenatal anxiety/depression/stress accounts for 10% attributable load of probable mental disorder in the population - Children of anxious group have increased SDQ (Strength and Difficulties Questionnaire) at all stages from Age 4-13) | High anxiety group have 12% of MD by Age 13 (compared to 7%)
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15
Q

What is the double-hit hypothesis in prenatal risk for future mental health problems?

A
  • Only those with genetic disposition AND anxious/depressed mothers develop Mental Illness in later life - GG polymorphism in COMT gene + Anxious mother had worst working memory at Age 8 - shows gene-environmental interaction
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16
Q

Why is the placenta important?

A
  • Filters all substances that cross mother fetus | Placenta has high levels of 11beta-HSD2 (at M-F blood interface)
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17
Q

What does O’Donnell et al 2012 say? (11beta-HSD2)

A
  • The more anxious the mother, the lower the level of 11beta-HSD2
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18
Q

Describe ethnic differences between stress and 11beta-HSD2

A
  • Stress —> Decreased 11beta-HSD2 and increased Glucocorticoid receptors BUT only in Caucasians (no difference in non-Caucasians)
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19
Q

What’s the correlation between amniotic cortisol and cognitive development score?

A
  • Increased amniotic cortisol —> decreased cognitive development score (at 17m) -1st shown by Bergmann, 2010 - Insecure attachment: Increased cortisol —> decreased cognitive score - Secure attachment: Increased cortisol —> no change in cognitive score
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20
Q

Describe fMRI study of antenatal stress

A
  • Antenatal stressful life events correlated with fMRI activation during rewarded attention
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21
Q

Describe epigenetic modifications of prenatal problems

A
  • Maternal prenatal depression associated with methylation pattern in infant cord blood, Teh, 2014 - Prenatal pregnancy specific anxiety associated with epigenetic changes in infant cord blood, Hompes, 2013 - Epigenetic change can transfer stress up to 3rd generation
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22
Q

Why is prenatal stress related to neurodevelopment?

A
  • Evolutionary advantage: Predictive-adaptive response (e.g. child with anxiety has increased vigilance —> more likely to detect dangers) - Sex differences: Females look after Offspring (Increased rates of anxiety), Males explore and fight (increased rate of conduct disorder) - Dose response effect between stress and risk | Not all children affected in the same way (genetic basis for natural selection)
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23
Q

What are roles of professionals in helping mothers?

A
  • Detect and treat anxiety and depression both in pregnancy and postnatally - Psychological interventions (eg CBT) - Pharmacological intervention if needed - Help with relationship problems or domestic abuse - Help to create more social support - Practical help with housing etc - Help to teach sensitive mothering – video feedback
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24
Q

What is self-harm?

A
  • NICE guidelines: “act of self-poisoning or self-injury, irrespective of apparent purpose of the act - E.g. cutting, burning, overdoses, punching a hand against a wall etc
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25
Q

What is Non-suicidal self injury (NSSI)?

A
  • “the deliberate damage to the body in the absence of (conscious) intent to die, and commonly includes behaviours such as skin cutting and self-battery” (Nock, 2009). “ - Similar to self harm
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26
Q

Is it important to differentiate between self-harm and NSSI?

A

PRO: Important to differentiate because - DIFFERENT case conceptualisation, risk assessment, treatment (e.g. hospitalisation) AGAINST: - NOT a dichotomy, but a multidimensional construct = ambiguity - Difficulty of a valid and reliable assessment of intent

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27
Q

What is the case for including NSSI in the DSM-5?

A
  • condition requiring further research - transdiagnostic nature of the behaviour and not just in borderline personality disorder (BPD) - clinical and functional impairment - NSSI purely within a BPD context or as a manifestation of suicidality will hamper research and treatment of NSSI
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28
Q

Which demographics are mainly self-harming?

A
  • 25.7% of 16 to 24 year old women reported having self-harmed at some point in their life - 9.7% of 16 to 24 year old men - 13.2% of women aged 25 to 34 - Report bias? May be acceptable for females to disclose self-harm than for males - Males may not associate some behaviours with self-harm e.g. punching a wall
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29
Q

What is the iceberg model of self-harm?

A
  • 15–17 years females: for every suicide, 919 girls presented to hospital for self-harm and 6406 self-harmed in the community (without coming to the attention of health services) - (Geulayov et al., 2018)
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30
Q

Describe repetitionsof self harm

A
  • 1 in 4 still repeating after 4 years & increased severity (Moran et al., 2012) - Almost 1/2 of hospital presentations repeat SH in the following 6 weeks (Perry et al., 2012) - In a sample of adolescents participating in psychological therapy trial for depression: - Predictors of NSSI over 28 weeks of follow-up: baseline NSSI, hopelessness, anxiety disorder, younger age, female gender - Predictors of suicide attempts over 28 weeks of follow-up: baseline high suicidality, NSSI, and poor family function (Wilkinson et al., Am J Psychiatry 2011)
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31
Q

What are associated factors of self-harm?

A
  • Disadvantaged socio-economic background - Social isolation and lack of support - Negative life events including childhood emotional, physical or sexual abuse
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32
Q

Are there any predictors of self harm?

A
  • Weak longitudinal predictors model - Strongest predictors: prior history of NSSI, cluster B personality disorder and hopelessness (Fox et al., Clin Psychol Rev. 2015) - No replicated data and no longitudinal studies on cognitive measures either - Data limitations: - NSSI measurement, sample type, sample age, outcome measurement - Few studies among samples with an NSSI history (i.e. prediction of self-harm repetition)
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33
Q

What are risk factors for SH repetition?

A
  • Symptoms of depression, anxiety, substance abuse - Related to psychiatric disorders because of etiologic pathways? (Nock, 2009)
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34
Q

What are personality traits and psychological factors of SH?

A
  • Sense of entrapment - Lack of belonging/perceiving oneself as a burden - Low self-esteem - Impulsivity - Hopelessness
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35
Q

Why is self-harm a problem?

A
  • Increased suicidal thoughts/attempts and death on top of the risk conferred by the presence of mental illness and by psychosocial risk factors - index of distress and poor mental health: 20 years community-based longitudinal study: SH marker of adolescent distress & indicator of poor long-term outcomes - poor health and functional outcomes (Mars et al., 2014) - substantial personal impacts (shame, guilt, and physical damage costs) on individual and family - poor educational & vocational outcomes (Cox et al., 2017)
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36
Q

What is the association between self-harm and suicide?

A
  • Association stronger among individuals engaging in more severe forms of NSSI (cutting) - Shared factors associated with NSSI and suicidal behavior: sociodemographic factors (possibly: impulsivity, abuse history) - Distinct factors: greater psychopathology and worse psychosocial functioning in suicidal behaviour (possibly: greater depression & hopelessness ?)
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37
Q

What is the Gross emotion regulation model? (self harm)

A
  • Gross emotion regulation model: reappraisal vs suppression (Gross and John, 2003) - Increased emotional suppression - Cognitive reappraisal leads to less frequency and medical severity in NSSI
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38
Q

What is Gratz and Roemer’s “difficulties in emotion regulation” model?

A
  • Based on Linehan’s work with BPD - awareness and understanding of emotions [alexithymia] - acceptance of emotions - ability to control impulses and behaviour in accordance with goals - ability to be flexible in using situationally appropriate strategies - Deficits in facial expression recognition - Increased self-reported impulsivity
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39
Q

What is the Chapman’s “experiential avoidance” model? (Self Harm)

A
  • Avoiding emotions - Self harms helps to avoid emotion - Temporary relief causes negative enforcement and vicious cycle - SH becomes automatic response to when you want to avoid an emotion
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40
Q

What is the Selby & Joiner “emotional cascade” model?

A
  • Rumination amplifies negative emotion and self harm interrupts this cascade - Increased rumination associated with self harm
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41
Q

Is self-harm an addictive process?

A
  • Majority of self-harm individuals had 5 or more endorsements when substance abuse questionnaire adapted for self harm (Nixon et al, 2002)
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42
Q

How is self-harm and substance abuse?

A
  • Evidence of risky decision making - Attentional biases to cues - High impulsivity
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43
Q

What is the evidence that self-harm individuals have reward processing abnormalities?

A
  • People who were self-harming didn’t adopt the low risk strategy as much as the people who stopped for more than a month - If self-harm was helpful but no longer helpful anymore, unable to spot
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44
Q

Describe SH and reward anticipation

A
  • SH individuals had reduced activation to money reward cues - Consistent with addict population
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45
Q

Describe SH and sensitisation to self-harm images

A
  • SH individuals found self-harm images more arousing - Increased acrtivation in reward processing areas such as orbitofrontal cortex
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46
Q

Summarise SH and addiction

A
  • Psychological drivers of self-harm (subjective experience) suggest dysfunctional mechanisms for coping with emotional stimuli / negative affect - Phenomenology also similar to addiction (at least in some individuals) - On a cognitive levels: - dysfunctional emotion regulation - impulsivity? - initial evidence of dysfunctional reward processing
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47
Q

How does mental imagery affect SH?

A
  • The more they found the mental image of self harm distressing the less likely to act on the urge to self-harm - and vice versa - Imagingin the reward of achieving a goal can strengthen motivation to engage in the action - Imagery is also one of the volitional factors of suicidal behaviour - motivation to action - Imagery not only of self harm, also imagery of distress or trauma
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48
Q

What are the reinforcement mechanisms of self harm?

A
  • interpersonal positive reinforcement (i.e., NSSI facilitates help-seeking) - interpersonal negative reinforcement (i.e., NSSI facilitates escape from undesired social situations)
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49
Q

What are deficits in social problem solving and communication among self-injurers?

A
  • Social learning hypothesis: increase over the past decades (Whitlock et al., 2009) - Self-punishment hypothesis: self-directed abuse learned via repeated abuse or criticism by others (Glassman et al., 2007) - Social signalling hypothesis: when other communication strategies have failed / an unresponsive or invalidating environment (Wedig & Nock, 2007)
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50
Q

Describe aberrant pain perception in self-harm

A
  • Aberrant pain perception - Increased pain tolerance in individuals with SH (St Germanin & Hooley, 2013) - Higher pain threshold in adolescents with SH, not mediated by habituation / dissociation (Glenn et al., 2014) - Mediated by emotional dysregulation (Franklin et al., 2012)
51
Q

Describe the opioid dysfunctional theory in self-harm

A
  • acute SH to temporarily increase endogenous opioids - In BPD sample: SH group lower levels of CSF β-endorphin and metenkephalin compared with non-SH group, but not of serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), and dopamine metabolite, homovanillic acid (HVA)
52
Q

What are the neurofunctional abnormalities in self-harm?

A
  • Aberrant amygdala activity and functional connectivity in response to emotional stimuli (Niedtfeld et al., Biol Psychiat 2010, Schreineret al., J Affect Disord 2017) - Dysfunctional activity during emotion regulation but not emotional reactivity vs. depressed individuals (Davis et al., 2014) - Physical pain task: In SH individuals greater relief after self-administered painful stimuli = activity in areas involved in pain/reward in addiction: thalamus, dorsal striatum and anterior precuneus. (Osuch et al., 2014) - In a social exclusion paradigm: - depressed adolescents with SH = enhanced activation of mPFC and vlPFC compared to depressed adolescents without SH (and also compared to healthy controls). (Groschwitz et al., 2016)
53
Q

What psychological therapies are used in CBT for self-harm?

A
  • Adaptations to CBT - Think differently to situations and reappraise situations - Emotional regulation techniques - Distress tolerance techniques - Problem-solving interventions - Social support - Interpersonal therapy - LIMITATION: only done in trials with PD - Not everyone wants to do group therapy - Adolescents may not want to engage in full sessions
54
Q

What are clinical practice challenges to self-harm?

A
  • No immediate intervention available - “Not severe enough”: excluded from complex psychological therapy - “too risky” (e.g. overdose): excluded from short psychological therapy - Transition from CAMHS to adult services: further challenge
55
Q

What are some digital interventions for SH?

A
  • BluceIce - Imaginator - My Self-Help Tool
56
Q

What is personality?

A
  • Enduring (long-term) pattern of perceiving, relating to and thinking about the environment and oneself - Pattern of thoughts, feelings and behaviour | Personality is revealed by behaviour | Flexible (vary to situ)
57
Q

What is personality disorder?

A
  • a set of personality traits that are pervasive, ingrained, maladaptive and create significant functional impairment or subjective distress
58
Q

What is Eysenck’s personality theory?

A
59
Q

What are the Big Five Personality traits?

A
  • Openness: Emotional | Curious
  • Conscientiousness: Self-disciplined | Result-orientated
  • Extraversion: High energy level | People person (stimulated by being around others)
  • Agreeableness: Co-operative | Able to forgive
  • Neuroticism: Sensible | Sensitive
60
Q

What is the ICD-10 Classification of personality disorders?

A
  • F60.0 Paranoid
  • F60.1 Schizoid
  • F60.2 Dyssocial (antisocial)
  • F60.3 Emotionally unstable (borderline)
  • F60.4 Histrionic
  • F60.5 Anankastic (Obsessive-Compulsive)
  • F60.6 Anxious (Avoidant)
  • F60.7 Dependent
61
Q

What is Cluster A personality?

A
  • Odd and eccentric, introvert-like, suspicious of others (stay away from MH services)
  • Paranoid: super-introverted, social withdrawal
  • Schizoid: do not trust others
62
Q

What is Cluster B personality?

A
  • Flamboyant and dramatic, Emotional instability, Aggressive (Borderline PD seek help from MH services due to self harm)
  • Antisocial: exploit others with guilt (Conduct disorder may be a precursor) (Associated with harms to others)
    3 of 7: Failure of social norms | Deception | Impulsivity | Irritability
  • Borderline: Mood swings, Impulsivity (Associated with self harm)
    5 of 9: Difficulty controlling anger | Chronic feelings of emptiness | Affective instability | Impulsivity
  • Histrionic: Over-dramatic, craves attention
63
Q

What is Cluster C personality?

A
  • Anxious and fearful (Dependent PD seek help from primary care)
  • Obsessive compulsive
  • Anxious: want to have friends but shy, socially isolated due to fear of rejection
  • Dependent: low self-esteem, reliant on others
64
Q

What is the ICD-11 classification of personality disorders in terms of severity?

A
  • Difficulty: present but not associated with pervasive dysfunction
  • Mild: limited interpersonal dysfunction
  • Moderate: marked dysfunction, in more than one cluster, clear risk to self others
  • Severe: severe dysfunction, more than one cluster, severe risk (endangering life)
65
Q

How to assess personality?

A
  • Use information from personal, employment social and forensic history
  • Start with a general question: ‘I would like to ask you some more questions about the sort of person you generally are’
  • ‘How would people who know you describe you?’
  • Try to interview the person on more than one occasion
  • Interview a relative or friend who knows the person well
  • Documentary evidence e.g. police contacts
  • Validated semi-structured interviews (SCID, IPDE)
66
Q

Which personality disorders are mainly influenced by temperament?

A
  • Schizoid
  • Anxious
  • Emotionally unstable
67
Q

Which personality disorders are mainly influenced by environment?

A
  • Anti-social
  • Paranoid
  • Emotionally unstable
68
Q

Describe the Swedish adoption study

A
69
Q

What is the aetiology of personality disorder?

A

•Environment > genetic

Except impulsiveness and cluster A

•Unstable family background – NEGLECT

Parental mental illness/drug misuse, social care

•Childhood physical and sexual abuse

The response of caregivers to abuse

70
Q

What are the consequences of inavoidant and ambivalent attachment?

A
  • Poor development of a sense of self
  • Self hatred and self harm

Impairment in:

  • Ability to tolerate distress
  • Ability to calm yourself
  • Ability to stop and think and consider alternatives
  • Ability to trust others
  • Ability to trust yourself
  • Knowing how to express needs (scream or withdraw)
71
Q

What is the prevalence of personality disorder?

A
  • Community (3-12%)
  • Primary care (27-33%)
  • Psychiatric clinics (35-50%)
  • Prisons (70-80%)
72
Q

What is the relationship between prevalence of PD and rates of homicide?

A
  • Positive correlation
73
Q

What are the course and consequences of personality disorders?

A
  • “Ingrained”
  • Over 20 years - cluster A and C increase (paranoia, rigidity and stubbornness)
  • Cluster B improve – decreased impulsivity and self-harm (50% ‘recovered at 2 years, 80% at 10)
  • 40% of people who die by suicide
  • 70% of people with drug dependence
  • 60% of prisoners
  • Reduced life expectancy (18 years)
74
Q

What are the principles of management of personality disorder?

A
  • Staying calm- containing anxiety
  • Acknowledge distress
  • Find out what’s going on
  • Avoiding extremes e.g. dismissing - taking over
  • Active participation of patient in working out what to do (what helped in the past?)
  • Being consistent as a service
  • Know your limits and boundaries
75
Q

What is mental illness?

A
  • Impairment of an individual’s normal cognitive, emotional or behavioural functioning (implies failure of a part of the body)
76
Q

What is a disorder?

A
  • disruption in functioning
  • broader term including psychologicaland psychosocial functioning
  • does not imply change in functioning
77
Q

What are cons of personality disorder diagnosis?

A
  • Mislabelling social advance
  • Diverts limited resources from those who need them most
  • Undermining personal responsibility
  • Creating dependency
78
Q

What are the pros of a diagnosis of personality disorder?

A
  • Helping inform patients and relative
  • Guiding patient management
  • Avoiding treatment that don’t work
  • Being able to offer treatment that do work
79
Q

What is fundamental attribution error?

A
  • The tendency of people to place an undue emphasis on internal characteristics to explain someone else’s behaviour in a given situation rather than considering the situation’s external factors
  • When explaining one’s own behaviour, people are more likely to highlight situational factors
80
Q

What are challenges of delivering psychological treatments for personality disorders?

A
  • Lack of trust
  • Affective instability
  • Unstable relationships
  • ‘frantic efforts to avoid abandonment’ (treatment ending)
81
Q

What are the consequences of insecure attachment?

A
  • Poor sense of self
  • Development of poor social and emotional skills
  • Development of maladaptive cognitions
82
Q

What is mentalising

A
  • Interpreting the actions of onself and others as meaningful on the basis of intentional mental states (e.g., desires, needs, feelings, beliefs, & reasons)
  • May be implicit (unconscious e.g. mirroring) or explicit (conscious e.g. interpreting). Subjective and inter-subjective (having the other persons’ mind in mind, as well as your own)
  • Thoughts are just thoughts…they are not ‘you’ or ‘reality’ (can help free someone from the distorted reality that thoughts create). It promotes openness and mentalization.
83
Q

What is contigent mirroring?

A
  • The caregiver accurately matches the infant’s mental state and ‘marks’ it to indicate that they are not expressing their own feelings
  • Incongruent mirroring: representation of internal state corresponds to nothing real —> pretend mode
  • Un-marked mirroring: caregiver’s expression seen as externalisation of experience —> psychic equivalent mode
84
Q

Describe Mentalisation Based Treatment for personality disorder?

A
  • Modified psychoanalytical psychotherapy | Individual and Group work | 2x weekly for 18 months
  • Ask about patient’s understanding of motives: “Why do you think he said that he..” - promoting intepreting actions
  • Group-based discussions: Group talks about difficulties and Therapist identifies when not mentalising and promotes it
  • “Stop, Listen, Look” - identify how it could be viewed from other people’s perspectives - “How do you think X feels?”
  • “Stop, Rewind, Explore” - if heated/uncontrolled argument, leave it for now and follow up next week when calmer (increased mentalisation)
  • Evidence: decreased suicide, decreased self-harm, increased social function
85
Q

How does maladaptive cognitions develop>

A
  • Schema – superordinate/ organising…how people organise and make sense of their world
  • ‘Generals’ of information processing
  • Adaptive - processing information in the context of neglect/ trauma
  • Maladaptive - when the context changes and these linked thoughts impair functioning
  • Dependent: I am helpless —> trying to cling to other Paranoid: Other people are a threat —> vigilance
86
Q

What is Schema Focussed Therapy?

A
  • Modified CBT – early maladaptive schema
  • Longer duration and intensity 2x week 18-24 months
  • People seek consistency and predictability. Schema help people make sense of something new.
  • Identification and exploration of the role of these ‘higher order’ cognitive processes in individual sessions or in a group.
87
Q

What is Dialectical Behavioural Therapy?

A
  • Mindfulness: The capacity to pay attention, non judgmentally, to the present moment - living in the moment.
  • Interpersonal effectiveness Strategies for asking for what you need, saying no, and coping with interpersonal conflict.
  • Distress tolerance: The ability to accept, in a non judgmental fashion, both oneself and the current situation
  • McMain found no difference compared with general psychiatric care
88
Q

Describe problem-solving therapy

A
  • Psychoeducation: up to four sessions of information and dialogue about personality disorder with the aim of building rapport, improving knowledge, and motivating participants for problem solving therapy.
  • Problem solving therapy is a 12-session group intervention designed to help participants learn a process for solving interpersonal problems.
89
Q

How does problem solving therapy work?

A
  • Identifying negative feelings -using these as a cue for the problem solving process
  • Define problem > specific goals for change > generating options > considering consequences > testing these out
  • Reducing ‘negative problem orientation’
90
Q

What were the results of the problem-solving therapy for PD?

A
  • No difference in social functioning
  • No difference in depression
  • No difference in three main problems
  • Increase in adverse events (e.g. presenting to A&E and MH services) (not statistically significance)
91
Q

What are problems of problem-solving therapy for personality disorders?

A
  • May not be able to draw upon previous positive problem-solving ideas for the therapy
92
Q

What are NICE recommendations for PD treatment?

A
  • Avoid treatments of short term duration
  • Use an explicit and integrated approach which is shared with the service user
  • Frequency should be adapted to needs, but twice-weekly sessions may be considered
  • Frequency should be adapted to needs, but twice-weekly sessions may be considered
  • For women with borderline PD for whom reducing self harm is a priority consider a programme of dialectical behaviour therapy
93
Q

Why treat Personality Disorder?

A
  • Distress (self, to others)
  • Suffering
  • Stigma
  • High service use
  • Increased morbidity and mortality
  • 4-12% of adult population
  • Up to 40% among those in contact with secondary care MH services (Newton-Howes,G. 2010)
94
Q

What are general principles for the management of PD?

A
  • Empathy
  • Consistency
  • Empowering
  • Encouraging autonomy
95
Q

Are there licensed medications for BPD?

A
  • No
96
Q

What is the DSM-IV criteria for Borderline Personality Disorder?

A

5 out of 9

  • Affective: —> ? Depression —> Antidepressants
    Inappropriate intense anger or difficulty controlling anger

Chronic feelings of emptiness

Affective instability —> ? Bipolar —> Mood stablisers

  • Cognitive:
    Paranoid ideation —> ? Schizophrenia —> Anti-psychotics

Identity disturbance

  • Behavioural:
    Suicidal behaviour

Impulsivity

  • Interpersonal:

Efforts to avoid abandonment

Unstable interpersonal relationships

97
Q

What is the ICD diagnostic criteria for BPD?

A

3 of 5

  • Impulsivity
  • Affective instability
  • Inability to plan ahead
  • Intense anger
  • Lack of sense of control
98
Q

What is the current evidence for the effectiveness of antidepressants on personality disorder?

A
  • n=7 trials
  • 6 trials show no benefit, co-morbid PD and depression. 2x increased poor outcome for depression (rarely work)
99
Q

What is the evidence for the effectiveness of anti-psychotics on personality disorder?

A
  • n=13 trials
  • Some evidence of decreased anger and impulsivity BUT side effects (weight gain), methodological issues
  • Helpful in terms of crisis | Only short-term use | Must explain prior to prescribing that is this short-term only
100
Q

What is the current evidence of the effectiveness of mood stabilisers for personality disorder?

A
  • n=9 trials: (1) Carbamazepine, (3) Valproate, (3) Topiramate, (2) Lamotigine
  • evidence of decreased anger and impulsivity BUT methodological issues and small trials
101
Q

What does NICE and Cochrane say about the use of drug treatments for personality?

A
  • NICE Guidelines discourages drugs for BPD BUT Cochrane review recommends mood stabilisers and 2nd generation anti-psychotics
102
Q

Why do NICE and Cochrane Review have differing opinions on providing drug treatments for personality disorder?

A
  • Interpretative bias (methodological quality)
  • Cost/benefits – weight gain, teratogenesis (IQ and valproate)
  • Difference between clinical and research populations
  • Compliance
  • Overdose
  • Polypharmacy
103
Q

Describe the the Audit in 3 London Mental Health trusts for drug treatment of personality disorder

A
  • 50% Borderline PD patients on antidepressants despite no Dx of depression
  • Lower levels of medication among those treated by specialist PD services
104
Q

Describe the Prescribing Observation for Mental Health (POMH-UK) for drug treatment of personality disorder

A
  • 1 in 3 Borderline PD prescribed more than one antipsychotic
  • Those who did NOT have an axis one disorder recorded, there was LESS likely to have documented evidence of check for side effects
105
Q

Why else do NICE discourages drug treatment for personality disorder?

A
  • Life expectancy reduced by 19 years – main cause cardiovascular disease (Fok et al. 2011)
  • Cost: £7000 per patient (Glen-Baker et al. 2010)
  • Psychological treatments work but many don’t want them
  • Many (including most severe) considered unsuitable
  • 20-50% drop out before completion
  • Need for better evidence about value of drug treatments
106
Q

Describe the LABILE study

(Lamotrigine for Borderline PD)

A
  • Na+ channel blocker | Used to treat epilepsy and bipolar disorder | Mood stabiliser | Limited S/E | No overdose | Less than one in 1000 get severe rash - fatal if not treated
  • Results: No difference between Lamotrigine and Placebo
  • Strengths: Largest ever trial of mood stabilisers, good follow-up rate (70%), independent randomisation, independent data monitoring committee, used validated measure of severity of Borderline PD (ZAN-PD scale)
  • Limitations: More clinical attention than normal clinical practice - more regular follow-ups
107
Q

Why are drug prescribing rates so high in personality disorder?

A
  • Patient: Fear of abandonment | Lack of trust
  • Clinician: Counter transference: patient may arouse anger (doing harm) feeling you are not doing enough
  • Feelings of hopelessness —> urge to prescribe, Evans, 2014
108
Q

What are principles of management for personality disorder?

A
  • Staying calm - containing anxiety
  • Active participation in working out what to do (what helped in the past?)
  • Avoid extremes
    e. g. dismissing-taking over, excusing-demonising
  • Being consistent as a service (reflective practice)
  • Knowing your limits and boundaries, (while avoiding extremes)
109
Q

How do you evaluate the use of medication for personality disorder?

A
  1. Be explicit – there is no drug licensed for your condition
  2. Actively involve the patient – what can they do, what has helped in the past
  3. Consider the context and meaning of requests for medication (…………more later)
  4. Consider reasons for an impulse to prescribe (counter-transference) reflective practice?
  5. Containing anxiety – arrange a follow-up appointment if you can deliver this
  6. Voluntary sector/ NHS helplines
  7. Avoiding extremes (denying comorbidity/ poly-pharmacy)

> Review and STOP medications prescribed during crises <

110
Q

What is stigma?

A
  • Distinguishing personal trait perceived as physically, socially or psychologically disadvantageous
111
Q

What is ignorance?

A
  • Lack of knowledge
112
Q

What is prejudice?

A
  • View formed without adequate knowledge
113
Q

What is discrimination?

A
  • Prejudice influencing behaviour
114
Q

What is the first study on stigma?

A
  • Nunnally 1st recognised stigma in 1960s
  • Mentally ill people regarded with fear, distrust and dislike by the general public
115
Q

What did the UK Department of Health find out about people’s perceptions on mental illness in 2010?

A
  • 1 in 10 don’t want to live next to someone who has a mental illness
  • BUT attitudes are improving
116
Q

How does the media exacerbate stigma?

A
  • Newspaper articles about Schizophrenia often associated with dangerousness- Chopra, 2007
  • Crime stats: only 5% of murders are committed by Mentally ill people
117
Q

What is the impact on stigma (on the stigmatised)?

A
  • 50% avoided telling others- Wahl, 1999
118
Q

What are ways of reducing stigma?

A
  • Public Education | Social Norms
  • Social contact Theory: contact with objects of stigma is most powerful way to reduce stigma- Allport, 1954
  • Those with an increased frequency of contact negatively correlates with perceived dangerousness and desired distance- Link, 2003
  • Time to Change Project (2009): Increased contact, Mass Media Campaigns, significantly reduced stigma towards MI (DofH)
119
Q

What is Coercion?

A
  • Forcing someone to do something against their will
120
Q

What does the Mental Health Act (2007) state?

A
  • Person can be kept in a psychiatric hospital against their will if they are a danger to themselves or to others
  • Decision made by an Approved Clinician based on experience and CARDS Risk Assessment (ever/never, don’t know)
  • Section 2: For assessment —> up to 28 days | Section 3: For treatment —> up to 6 months
121
Q

What do Community Treatment Orders do (2008)?

A
  • Must take treatment in community or will be sectioned even if no Sx
  • In response to “revolving door patients” who relapse, hospitalise with Tx, discharge, stop taking Tx, come back…etc
  • Section 17 Leave: High risk patient closely monitoring in community and re-admitted with Sx of relapse (Less coercive)
  • OCTET trial: CTO vs S17L: CTO did not significantly reduce re-hospitalisation compared to Secion 17 leave
122
Q

What is the Mental Capacity Act (2005)?

A
  • 3rd parties have the right to make a decision on behalf to those who lack capacity (decision-specific)
  • To have capacity, need to be able to [1] Understand, [2] Retain, [3] Weigh Up and [4] Communicate information
  • However under the Mental HEALTH act, there is no requirement to assess capacity in order to treat them regardless
  • This is biased as one cannot be forced if treating a physical illness
123
Q

How to increase capacity in Mental Illness?

A
  • 60 minute educational intervention enhanced capacity of Schizophrenia to same as controls- Carpenter, 2010
124
Q

What is an Advanced Directive?

A
  • Statement of wishes regarding treatment should capacity be lost in the future
  • Often not used (10% psychiatric outpatients have Advanced Directive, this increased to 60% when Advanced Directive explained to patient) - Swanson, 2006
  • However under Mental Health Act can override Psychiatric Advanced Directive (except for electroconvulsive therapy)
  • Mental Act Capacity Code of Practice recommends clinicians comply with PADs and document non-compliance