Psychopathology Flashcards

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1
Q

What is normal?

A

○ Could be:
§ being part of majority (not an ideal definition) (part of normal curve)
§ Autonomous functioning
§ Accurate reality perception
§ Regulated moods
§ Adequate interpersonal relationships

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2
Q

Why is the idea of abnormal difficult to define?

A

○ Statistical infrequency?
§ Difficult because if someone is abnormal in one domain (eg super smart), they could also be abnormal in a bad domain (eg poor interpersonal skills)
○ Norm violation?
§ In the past, the idea of a social norm has radically changed (eg views on homosexuality), so difficult to base a definition on this
○ Personal distress
§ What causes people to distress varies a lot
§ Very subjective
○ Disability/dysfunction
§ But we can change how we define what determines a disability or dysfunction

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3
Q

What was the early conception of mental illness?

A

people were a threat to public order
○ Viewed as a moral failing or a spiritual failing, or a physical failing - body or brain
§ No in between - no accpetance of the idea of the psychological or mental - either moral or physical
§ Majority of admissions into asylums were police, 1/3 were family members who couldn’t care for relatives
§ Many aslyums had to close because they became overpopulated
○ Because the focus was on the threat to public safety, there was little care for the wellbeing or recovery of the individual
§ Treatments were very experimental and inhumane
§ Occurrences of ‘shell shock’ (PTSD) in soldiers after WWI showed that ‘normal’ individuals could succumb to nervous illnesses
□ Created desire for more humane treatment
§ Anti-psychiatry movement prompted interest in non-invasive, more humane interventions

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4
Q

Describe de-institutionalisation

A

○ Amount of people in insititutions in AUS started declining rapidly in 1950s
§ At first this occurred because many facilities started using treatments that actually worked
□ Open-door policies - people could come in, get treatment, and go home
§ Second shift occurred (stage 2) - closing of the asylums because people did not think it was appropriate
□ Treatment moved to community - community hospitals, treatment centres etc

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5
Q

How has treatment of mental illnesses changed since 1950s?

A

○ Early on, predominantly private specialists managed treamtents in the asylums
○ By 1990, majority of treatment was done by GP (majority) or community providers

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6
Q

What is mental disorder?

A

○ Clinically significant disturbance in an individual’s cognition, emotion regulation, or behaviour … usually associated with significant distress or disability in social, occupational, or other important activities
§ DSM V

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7
Q

What is not a mental disorder?

A

○ An expectable of culturally approved response to a common stressor or loss, such as the death of a loved one
§ DSM V

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8
Q

What is the case against diagnoses?

A

○ Leads to bias or restricted thinking
§ Diagnostic boundaries are rarely distinct and diagnoses change over time
○ Are associated with jargon
§ Are clinicians in fact thinking about the same construct? Jargon may mask what is actually being discussed
○ Inhibit research
§ See the case for the RDoC
§ If we only study conditions meeting specific criteria, we may be missing a larger part of the picture
○ Can be stigmatising and have personal implications
§ How does this effect existing experience? If a brain disorder, is the brain ‘broken’? If it’s not a brain disorder, is something wrong with ‘you’?
○ Some people contend that mental disorder is a myth
§ Thomas Szasz
□ General thesis
® Psychology and psychiatry rely on an assumption that emotional distress, family, and personal turmoil are societal constructions
® This is an unproven hypothesis that is actively promoted by drug companies etc to make people behave in the way they want
□ Response
® Kendler
◊ Few cases seem to be entirely socially constructed

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9
Q

What is the case for diagnoses?

A

○ Facilitate communication
§ Among clinicians, between science and practice
○ Facilitate care
§ Identification of treatment, and prevention of mental disorders, description of experience, possible etiology and prognosis
○ Researcg
§ Test treatment efficacy and understand etiology
○ Education
§ Teach psychopathology
○ Information management
§ Measure and pay for care

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10
Q

Define sign

A

○ Objective findings observed by a clinician

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11
Q

Define symptom

A

○ Subjective complaints reported by a patient

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12
Q

Define syndrome

A

○ Signs, syndromes, and events that occur in a particular pattern and indicate the existence of a disorder
○ Can be a disorder but doesn’t need to be

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13
Q

Define disorder

A

○ A syndrome which can be discriminated from other syndromes
○ To be labelled a disorder means there is a distinct course to the syndrome and the age and gender characteristics of the disorder have been described
In some cases, prognosis may also be known

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14
Q

Define disease

A

○ For a disorder to be labelled a disease, there has to be indications of abnormal physiological processes or structural abnormalities

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15
Q

What are some assessment methods of psychopathology?

A
  • Pen and paper tests
    • Clinical interviews
    • Behavioural assessment
    • Activity diaries
    • Psychologial tests
    • Medical tests
    • Psychophysiological tests
    • Neurophysiological tests
    • Context is important
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16
Q

What are the dominant classification systems?

A

• Categorical systems of ICD and DSM

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17
Q

Describe the anti-psychiatry movement

A

• 1960s movement away from the way in which psychiatry was being practiced
• 1950s was when people started getting institutionalised and treatments
• Foucalt argued that treatment was largely about forcing individuals to conform
• Thomas Szasz believed that psychiatric treatment was a means by which to punish deviance from societal or moral norms
○ Further argued that diagnoses were not meaningful and that they were used to justify inappropriate treatments
• Many advocates for the movement argue that sociocultural factors are a major determinant of problems
○ Ie problems are resulting from shifts within subsections of society that are undesired by others
• This movement has led to the modern lived experience movement
○ There has been a recognition over time that people with a lived experience should be involved in how they’re treated and what they do

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18
Q

What are the three approaches to classification?

A

○ Categorical
○ Dimensional
○ Hybrid

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19
Q

Describe the categorical approach to classification

A

§ Divides psychological disorders into categories based on criteria sets with defining features
§ Used by ICD and DSM
§ Better clinical and admistrative utility - clinicians are often required to make dichotomous decisions
§ Clinical resources are limited
§ Easier communication

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20
Q

Describe the dimensional approach to classification

A

§ Aspects of psychopathology are quantified on a scale
§ Where does a person fall on the continuum
§ Closely model lack of sharp boundaries between disorders and normality
§ Can develop treatment-relevant symtom targets - not simply aiming at resolution of disorder (most treatments target symptoms not disorders)

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21
Q

Describe the hybrid approach to classification

A

§ A hypothetical combination of categorical and dimensional
§ Could look like: people above this threshold fit into this category, but below that they do not
§ In theory it is the best of both
§ Examples of hybrid
□ MMPI personality inventory
® Have multiple questions on various categories
® Add up those responses and scale it based on normal distribution
® Comes up with a profile of roughly where they stand for each category, so you can see certain areas which might need more support etc

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22
Q

What are the three major movements in clinical psychology?

A

○ First started with Freud
○ Behaviourist movement
○ Cognition/thoughts

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23
Q

Describe the Freudian paradigm

A

§ 1856-1939
§ Freudian paradigm
□ Ego
® Main representation of self
® Part of self that interacts with external world
® Influences on ego and superego and id
□ Superego
® Sense of morality
□ Id
® Desires
□ The unconscious has a huge influence on what we do dayy-to-day
□ Only by choosing to become aware of unconscious motivations can individuals choose less maladaptive and more adaptive behaviour
□ Criticism
® Just being aware of unconscious impulses does not necessarily mean the person does anything about them

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24
Q

Describe the behaviourist movement

A

§ Skinner
§ 1904-1990
§ Focusing on only things we can observe
§ Focusing on objective things
§ Not too worried about thoughts or emotions
§ Behavioural paradigm
□ Approached individuals like input/output machines
□ Didn’t matter what happened in our brains
□ What matters is the stimulus and response pairings
□ Goal of behavioural interventions is to interrupt/change stimulus-response associations
□ Skinner believed we would be best served by doing away with concepts like free will

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25
Q

Describe the cognition movement

A

§ Beck
§ Don’t have to focus on behaviours - can also focus on the way people think, behave in the world, and use them together
§ Cognitive models
□ CBT:
® The way we think and the way we behave have a fundamental relationship with the way we feel
® Thoughts, behaviour, and feelings are interrelated and to change one, you need to change the other two

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26
Q

What are the biopsychosocial models?

A

§ Integrates a range of factors
□ Biological
® Normal biology, disease processes, and genetic influences
□ Psychological
® Thoughts, feelings, perceptions
□ Social/environmental
® Culture, ethnicity, social environment
□ The combination of all these things influences what we do and the way we do them

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27
Q

What is the biological paradigm?

A

□ Focus on genetics
® Alteration in a single gene, part of a gene, or interaction between genes contributes to why individuals may develop a psychiatric illness
® Myth that we can idenitfy a single gene connected to a signle disorder
® In reality, genes probably play a role, but it is much more complicated than we thought
□ Structural brain damage (hard lesion)
□ Disordered physiology (eg inflammation processes and depression)
□ Neurochemistry
® Myth: a lack of neurotransmitter/too much of it can lead to mental disorder
® Reality: there can be different amounts of neurotransmittters across the brain, so there might be one area that has to little, and another that has the right amount, so treating the disorder with drugs that target the whole brain might not help
□ Functional connectivity impairments (soft lesion: eg schizophrenia)
® Idea is that we can look at how different areas of the brain interact with each other
® However, over decades of research, within the same person, the way the brain may speak to itself is not reliable

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28
Q

What are the social determinants of mental health?

A

§ Issues in broader society that may contribute to poor mental health in groups of people
§ Proximal factors
□ Most closely related to the individual
® Eg age, gender, ethnicity
§ Distal factors
□ Furhter away from the individual either in physical space or in concept
® Eg community, population, diversity,
§ It is really important to look at how these factors interact with the individual over the course of their life

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29
Q

What is the diathesis stress model?

A

§ Based on certain things, there is a diathesis (vulnerability, often in terms of personality). That vulnerability interacts with stress (not necessarily negative stressful things).
§ Resilience is particularly important factor - if someone is highly resilient, they are less likely to be affected by the stressor

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30
Q

Describe Research Domain Criteria (RDoC)

A

§ Intorduced in response to issues happening in research context of the National institutes of Mental Health in America
§ Was meant as a reform for how we do research
§ Wasn’t meant to be a clinically-oriented model or a classification model, but meant to allow us more freedom in the way we study mental disorders
§ Focus not on disorders but on problems
§ Domains
□ Negative valence
□ Positive valence
□ Cognitive systems
□ Systems for social processes
□ Arousal/regulatory systems
□ Sensorimotor
§ The way the model suggests we should focus on the domains is in the contet of time
§ All of the domains are situated in an environmental context
§ Within the individual, there are a range of focuses
§ The idea is to focus on all these elements within a particular domain to try to understand the whole process
§ Could then use this to come up with a profile for the individual
§ Example fo how it is used:
□ Tamminga et al.
□ Took people with schizophrenia, schizoaffective disorder, and bipolar disorder (psychosis is the common symptom)
□ Put them all together, and focused on their cognitive control and sensorimotor activity
□ Measured genetics, brain activity etc
□ Looked for different patterns in association with the symptoms
□ Could then group people based on similarities rather than their diagnosis
□ Idea is to classify people more specifically
§ Limitation
□ Hasn’t yielded any actionable activity yet

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31
Q

What is the hierarchical taxonomy of psychopathology?

A

§ Idea is that you can work at different levels to understand different aspects of the disorders and how they link to other disorders
§ Cam from the idea that having a certain genetic profile seems to confer generic vulnerability for psychopathology
§ People may exhibit problems across multiple domains

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32
Q

Describe the clinical staging model

A

§ Model adopted from cancer (stages reflecting the disease - progression)
§ Based on observations by Pat McGorry and Henry Jackson in schizophrenia
§ Focus on identifying those at risk and facilitating early intervention
§ Different from Stepped Care approach
□ Setpped care is an escalation of treatment
□ Clinical staging suggests you get treatment according to stage of disorder
§ Very clinical
§ Also aims to use more universal interventions that are less costly, less harmful, and less intense at earliest stages
§ Limitation
□ Only implies that people progress in a worsening way, rather than getting better, then relapsing etc

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33
Q

What is the transdiagnostic model?

A

§ Goal is to say that there is no unique underlying factor that is specific to any given disorder
§ Recognition of shared aetiological and maintenance factors
§ May account for high levels of comorbidity between disorders - such as anxiety and depressive disorders
§ May also provide an explanation for why diagnostic specific therapies are not effective for all sufferers

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34
Q

What is anxiety?

A
  • Generally characterised by fear and negative affect

* Internalised

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35
Q

Explain how anxiety links to behaviour

A

○ Historically anxiety disorders have been thought of as disorders of avoidance
§ Avoiding some experiece/threat
○ Fight, flight, freeze
§ The freeze response is often overlooked
§ Sometimes people with anxiety feel like they don’t know what to do - overwhelmed by things
○ Approach-avoidance conflict
§ Wanting to go somewhere/do something (approach motivation), conflicts with the fear of going
§ This conflicts manifests in freezing behaviour

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36
Q

Explain the link between anxiety and fear

A

○ Thought they were the same
○ Fear describes feelings that occur when a source of harm is immediate or imminent
○ Anxiety describes feelings that occur when the source of harm or threat is uncertain or distant in space or time (anticipatory)
○ The Fear Center model
§ Original idea: there is a clear fear cicuit in the brain (amygdala)
§ The fear response happens automatically to environemtnal stimulus with no cognition attached

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37
Q

What is the Two-System model of anxiety

A

§ If you recognise that fear and anxiety are different, than the Fear Center Model doesn’t make sense
§ Our understanding of the amygdala is now much more nuanced
§ Now think that the amygdala is responsible for knowing recognising valence - what should we be paying attention to, what is relevant?
§ This model suggests two circuits:
□ Defensive-survival circuit
® Engaging in automated escape/defense response
□ Cognitive circuit
® The evaluation of the circumstance leads to the fear, not the behaviour we engage with
® This brings in also the prefrontal cortex in underlying the fear experience as well as the amygdala
◊ Prefrontal cortex = consciousness, and did not used to be thought of a relevant in terms of the fear response
○ Rather than being automatic, conscious processing associated with threat/harm is critical to the understanding of anxiety disorders

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38
Q

Provide a brief overview of anxiety disorders in general

A

• Anxiety disorders are the most common disorders globally
○ Most common is specific phobia, followed by GAD
• 15-20% of people are likely to have experienced an anxiety disorder in the past year
• Disproportionately effect women
○ Roughly twice as many
• While they are considered to be relatively mild, anxiety and depression account for the largest number of Disability Adjusted Life Years within mental disorders
○ Because the impact may not be as big as schizophrenia or psychosis, but when you combine the fact that they can cause major distress and disruption with the fact that a lot fo people experience this disorder, it adds up
• Generic treatment
○ Anxiety disorders tend to respond better to psychotherapy than to medication, however, in certain circumstances, medication is favourable
○ Generic treatment for:
§ At risk of anxiety or mild anxiety
□ Watchful waiting
□ CBT (inc. internet-based/computer-based CBT) if worsening
§ Moderate anxiety
□ CBT or pharmacotherapy (antidepressant) or both
§ Severe or treatment-resistant anxiety
□ CBT and pharmacotherapy

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39
Q

Describe specific phobia

A

• Avoidance category
• DSM 5 description
○ Marked fear, anxiety or avoidance of specific circumscribed objects or situations
○ Fear is out of proportion to the actual threat posed
○ The individual recognises the symptoms are excessive or unreasonable
§ In ICD, but not in DSM - people don’t always recognise the unreasonableness
○ Typically persists for a least 6 months
○ Subtypes include animal, natural environment (eg heights or storms), blood-injection-injury (eg needles), situational (eg planes), or other phobias
• Lifetime prevalence from 3-15%
• In youth, it is much more common, and then dies down until about 65/70 when it spikes up again for women

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40
Q

What is the aetiology of specific phobia?

A

○ Tend to develop through classic associative learning
§ The fear may generalise to other similar objects
○ Most people don’t recall the direct exposure triggering the fear
○ People can indirectly learn fear through social learning
§ Watching someone else fear something
○ Some people also overrepresent memories of certain events (Flashbulb memories), where details of a trauma may be remember with much more clarity than other memories

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41
Q

What is the treatment of specific phobia?

A

○ Exposure therapy
§ Present the person with the thing they fear
§ Help them feel relaxed/calm in that situation
§ Trying to break link between fear and the stimulus itself
§ Types
□ In Vivo
® In real life
□ Imaginary
® Picturing the object
□ Virtual Reality
® Simulation
□ Gradual
® Progressing to see the actual thing
® Might start by imagining, then drawing, then watch a video, then hold spider
□ Flooding
® Go straight to direct exposure ie suddenly putting spider on them
§ Difficult to do this therapy because many people don’t like it, but it is 70-85% effective
§ Premature termination of therapy is not uncommon

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42
Q

What is panic disorder?

A

• DSM 5 characteristics
○ Recurrent unexpected (eg occurring without a cue) and unavoidable panic attacks
○ Concern or worry about having more panic attacks or maladaptive behavioural changes
○ Persists for at least 1 month
• Epidemiology
○ 13.2% of population are likely to experience a panic attack in their lives
§ Among those with panic attacks, 66.5% report recurrent attacks
§ 4.9% past-year panic attacks
§ 12.8% of those with panic attacks meet for panic disorder
○ 1.7% of the population are diagnosed with panic disorder at some point in their lives
○ 1% of people were diagnosed with panic disorder in the last year
○ Most develop panic disorder between 18-29
○ Women 1.8x more likely than men
○ Low household income increases odds ratio 1:5

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43
Q

What is the aetiology of panic disorder?

A

○ Cognitive theories
§ Underpinned by catastrophic misinterpretations of somatic and other experiences
§ Counter arguments
□ Can induce panic attacks
□ Nocturnal panic attacks
□ Both of these indicate that cognition is not necessary
○ Anxiety Sensitivity Theory
§ Certain people are likely to be predisposed to be more sensistive to kinds of somatic experiences associated with panic attacks
§ Counter arguments
□ It is difficult to separate Anxiety Sensitivity from panic - does sensisitvity precede the panic attack?
○ Learning theory
§ Something people learn over time
§ Alarm theory
□ Start to sound the alarm the minute anything close to a panic attack happens
Eg exercising (increased heart rate, sweating, difficulty breathing)

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44
Q

What is the treatment of panic disorder?

A
○ Responds equally well with psychotherapy and pharmacotherapy
		○ Approaches that work
			§ CBT
			§ Antidepressants
			§ Benzodiazepines (antianxiety)
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45
Q

What is agoraphobia?

A

• Characteristics
○ Marked fear, anxiety, or avoidance of situations such as public transportation, open spaces, enclosed places, lines or crowds, or outside the home alone
○ Fears that escape might be difficult or help is not available in the event of panic-like symptoms or other incapacitating or embarrassing symptoms
○ Fear is out of proportion to the actual threat posed
○ Individual recognises symptoms are excessive or unreasonable
○ Typically persists for at least 6 months
• Epidemiology
○ Lifetime prevalence of 0.6-1.1%
○ Prospective studies have estimated closer to 5.3%
§ Following people over time - seeing if they end up fitting into the diagnosis
○ Debate about relationship between panic attacks and disorders
○ 46-85% of people with agoraphobia do not experience panic attacks
○ Course is usually chronic (only 10% experience full remission)
○ Most likely in people who are 45-59

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46
Q

What is the treatment of agoraphobia?

A

○ Very similar to panic disorder and specific phobias

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47
Q

What is social anxiety disorder?

A

• Characteristics
○ Marked fear, anxiety or avoidance of social interactions and situations in which one is scrutinised, or situations in which one is the focus of attention (eg being observed while speaking, eating, or performing)
○ Fear of negative judgement from others, in particular, fear of being embarrassed, humiliated, rejected, or offending others
○ Fear is out of proportion to the actual threat posed
○ Individual recognises the symptoms are excessive or unreasonable
○ Physical symptoms and symptoms of blushing, fear of vomiting, or urgency of/fear of micturition (peeing) or defaecation
○ Typically persists for at least 6 months
○ Social anxiety can be limited to performance situations only
• Epidemiology
○ 4% lifetime prevalence
○ 2.4% past-year prevalence
○ 1.3% past-month prevalence
○ 75% developed before age 20
○ 47% lifetime comorbidity with mood disorder
○ 59.8% lifetime comorbidity with another anxiety disorder
○ 26.7% lifetime comorbidity with substance use disorder
○ 38% receiving some treatment

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48
Q

What is the aetiology of social anxiety disorder?

A

○ Diathesis stress model
§ Genetic factors and environmental factors interact with proximal factors (behavioural and cognitive)
§ This interaction leads to the development of social anxiety

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49
Q

What is the treatment of social anxiety disorder?

A

○ Exposure therapy
§ Assumption is that the client has to experience the feared situation to change the affective-behavioural patterns and associative ideation
§ Can fail via mental distancing - “it’s just role play”
§ Safety behaviours (eg rehearsed speaking) can also be maladative
○ Applied relaxation
§ Progressive muscle relaxing may work
○ Social skills training
§ Can be helpful if there is a deficit
○ Cognitive restructuring
§ I must not appear nervous when public speaking -> I’d prefer not to appear nervous when public speaking

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50
Q

What is generalised anxiety disorder?

A

• Characteristics
○ Excessive anxiety and worry about various events that have occurred more days than not for at least 6 months
○ Difficulty controlling the worry
○ Anxiety and worry are associated with at least 3 of the following 6 symptoms (only one is required for children)
§ Restlessness or a feeling of being keyed up or on edge
§ Easily fatigued
§ Difficulty concentrating
§ Irritability
§ Muscle tension
§ Sleep disturbance
○ The anxiety, worry, or associated physical symptoms cause significant distress or impairment in important areas of functioning
○ The disturbance is not due to the physiological effects of a substance or medical condition
○ The disturbance is not better accounted for by another mental disorder
• Epidemiology
○ Global prevalence:
§ Lifetime - 3.7%
§ 12-month - 1.8%
§ Lifetime high-income countries = 5%, middle = 2.8%, low = 1.6%
○ Lifeitme comorbidity = 81.9% (Mood disorder = 63%, other anxiety disorder = 51.7%)
○ Severe role impairment in 50.6% of people with GAD
§ 28% at home, 32.1% at work, 31.1% relationships, 34.9% social
○ 49.2% seek treatment
○ Typical onset in late 20s/early 30s
§ 50% of casesappear prior to age 39, 75% by age 53
○ Chronic course: ~50% of people with lifetime GAD met criteria in past year

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51
Q

What is the aetiology of GAD?

A

○ Avoidance model of worry
§ Suggests that worry was an ineffective cognitive attempt to problem solve - removing a perceived threat while avoiding aversive somatic and emotional experiences
§ Counter arguments (after study)
□ Worry does not facilitate avoidance of emotions
□ Rather, worry does sustain negative emotionality (ie restricts affects)
® It may restrict the emotions you feel, so you generally may feel not great, but that means that there is not a huge drop in emotions when you start worrying
○ Intolerance of uncertainty model
§ Uncertain or ambiguous situations are stressful and upsetting. Belief that worry will serve to either help cope with feared events more effectively or to prevent those events from occurring at all
§ Problem
□ People don’t always believe that worry is helpful
○ Meta-cognitive model
§ People initially develop belief that worry helps (and perhaps it does), but subsequently begin to worry about their worrying (meta-worry). Efforts at thought control fail and people feel helpless
○ Emotion dysregulation model
1. Presence of more intense emotions, 2. poor understanding of emotion, 3. negative attitudes about emotions, 4. maladaptive emotion regulation

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52
Q

What is the treatment of GAD?

A

○ Only 50% respond to medications and/or psychotherapy
○ Insufficient evidence for meds vs CBT
○ Combined methods recommended in complex cases
○ Substance abuse comorbidity (35%)
○ Sleep problems comorbidity
○ Physical illness comorbidity
○ These comorbidities may explain why it is so hard to treat

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53
Q

What is the difference between unipolar and bipolar?

A

○ One step up from depression is dysthymia - a bit sad/persistently down or irritable
○ Euthymia = normal mood
○ Hypomania = slightly less than manic episode: feeling good but not amazing
○ Normal people have experiences between hypomania and dysthymia
○ Difference between bipolar and unipolar is that people with unipolar mood disorders only experience the negative dip - no presence of a positive affective state
○ Bipolar has this dip as well as experiencing a manic state

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54
Q

What is depression?

A

○ Can be a normal human emotion
§ Characterised by feelings of sadness, despair, unhappiness
○ Can be normal depending on the proportion of it
§ Grief
□ Appropriate sadness response to a recognised external loss
□ Uncomplicated bereavement - will end at some point
○ Complicated bereavement
§ Continue to be depressed/grieve for longer than what is seen as culturally appropriate
§ Difficult to diagnose - no two people grieve in the same way

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55
Q

When does normal depression become clinical depression?

A

○ Based on
§ Intensity
□ The mood change pervades all aspects of the person and impairs social and occupational function
§ Absence of precipitants
□ Mood may develop in the absence of any discernable precipitants or be grossly out of proportion to precipitants
§ Quality
□ Mood change is different from that experienced in normal sadness
§ Associated features
□ Mood change might be accompanied by a cluster of signs and symptoms including somatic and cognitive features

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56
Q

What is Disruptive mood diregulation disorder (DMDD)?

A

• Unipolar
• Epidemiology
○ Don’t know much about it because it’s relatively new
○ Estimated 3-month prevalence 0.8-3.3%
○ Highest rate in preschoolers
○ Co-occurrence with another psychiatric disorder 62-92% of the time
○ Very difficult to diagnose because it’s so common in young children and their moods fluctuate so much
• Characterised by
○ Extreme irritability
○ Anger
○ Frequent, intense temper outbursts
○ Not just being moody
○ Created in response to rise in diagnosis of bipolar disorder among children/adolescnece and inappropriate treatment of medication

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57
Q

What are the DSM5 criteria for DMDD?

A

○ Severe recurrent temper outbursts mnifested verbally and/or behaviourally that are grossly out of proportion in intensity to the situation or provocation
○ Temper outbursts are inconsistent with developmental level
○ Temper outbursts occur, on average, 3+ times a wek
○ The mood between temper outbursts is persistently irritable or angry most of the day nearly every day, and is observable by others
○ 12 month + duration - cannot have symptom-free interval of 3months+
○ Age of onset prior to 10 years

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58
Q

What is major depressive disorder?

A
• Gets diagnosed as an episode - get diagnosed with the disorder if they've had a depressive episode first
	• Major Depressive episode (MDE): 5/9 symptoms during 2 week period (most days)
		○ Depressed mood*
		○ Diminished pleasure & interest*
		○ Weight or appetites change
		○ Sleep disturbance
		○ Psychomotor disturbance
		○ Fatigue or loss of energy
		○ Feeling worthlessness or guilt
		○ Trouble concentrting or making decisions
		○ Recurrent thoughts of death
		○ *One of these two must be present
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59
Q

What is the epidemiology of major depressive disorder?

A

○ 12 month prevalence ~6% globally
○ Lifetime prevalence of 20.6%
○ 39.7% of cases = moderate severity
○ 49.5% of cases = severe
○ Ajusted odds ratio of also having generalised anxiety disorder: 5.7
○ 74.6% of cases were anxious distressed
§ Condition of the symptoms were best described by MDD - didn’t make sense to make diagnosis of both MDD and GAD, but also secondary to the depression is an anxious affect presentation which exacerbates the depressive symptoms
○ Depression was 2nd leading cause of Years Lived with Disability in 2010
○ Depression was leading cause of Disability Adjusted Life Years (DALY)
○ No real difference in how common it is in high or low socio-income countries

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60
Q

What are the associated problems and course of major depressive disorder?

A
○ Heart disease (rr=1.8)
		○ Diabetes mellitus (rr=1.6)
		○ Obesity (rr=1.6)
		○ Cognitive impairement (rr=1.8)
		○ Disability (rr=1.7)
		○ Cancer (rr=1.3)
		○ Mortality (rr=1.8)
		○ rr= risk ratio
	• Course
		○ 40-60% of people with depression exhibit stable recovery
		○ As many as 50% of individuals relapse within 5 years
		○ ~15% of individuals exhibit chronic course
		○ 30-60% exhibit recurrent course
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61
Q

What is the treatment of major depressive disorder?

A

• Treatment
○ CBT
○ Behavioural action therapy
§ Getting people to be active
○ Psychodynamic therapy
§ Inspired by Freudian approaches
○ Problem-solving therapy
§ Methods to identify particular problems and coming up with greater responses to them
○ Interpersonal therapy
§ Thinking about relationships, an getting people to engage socially
○ Mindfulness-based therapy
○ Medications
§ Insufficient amount, or too much of a particular neurotransmitter
□ Big three for depression
® Serotonin
® Dopamine
® Noradrenaline
§ Most common medical treament of depression is a selective serotonin reuptake inhibitor
□ Creates more serotonin in the brain
○ Treatment response
§ STAR*D study
□ Started people off with an SSRI
□ Then if they didn’t respond to that, progressed them to another form of treatment
□ Problem was, as people went to more and more stages, more people dropped out
□ The other problem, was that the likelihood of responding to a medication reduced as they got further along the progression
® This describes treatment-resistant depression: once you have tried a certain number of treatments, you start getting treatment-resistant

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62
Q

Describe suicide

A

• As many as 60% of people who commit suicide have MDD
• 12-month prevalence of suicidal ideation is ~2.0%
• 12-month prevalence of suicide attempts is ~0.3%
• Risk factors
○ Family history (OR 1.7-10.6)
○ Early life adversity
○ Psychiatric illness - esp depression, anxiety (90% of those who suicide)
○ Impulsivity
○ Substance misuse
○ Sense of hopelessness/helplessness
• Three stages of factors
○ Distal or predisposing
§ Eg family history/genes
○ Developmental or mediating
§ Eg personality traits, or elevated anxiety
○ Proximal or precipitating
§ Suicidal behaviour

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63
Q

What is persistent depressive disorder?

A

• DSM 5 Criteria
○ Depressed mood more days than not for at least 2 years
○ Presence of 2+ of the following
§ Change in appetite or weight
§ Change in sleep
§ Low energy or fatigue
§ Low self-esteem
§ Poor concentration or difficulty making decisions
§ Feelings of hopelesness
○ Previously known as dysthymia - low level, chronic depression
○ Proposed alternative to MDD

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64
Q

What is the treatment of persistent depressive disorder?

A

○ Generally the same as MDD
○ More likely to be treatment resistant
○ Physical and psychiatric comorbidities common
○ Undertreatment is likely as many people present to GPs

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65
Q

What is premenstrual dysphoric disorder?

A

Depressive disorder
• Minimum of 5 total (at least 1 each from A and B) in final onset of menses
• A)
○ Marked affective liability (eg mood swings, sudden sadness, increasing sensitivity to rejection)
○ Marked irritability, anger, or increased interpersonal conflict
○ Marked depressed mood, feelings of hopelessness, or self-deprecating thoughts
○ Marked anxiety, tension, or feelings of being keyed up or on edge
• B)
○ Decreased interest in usual activities
○ Difficulty concentrating
○ Lethargy, easily fatigued, lack of energy
○ Change in appetite, eating, cravings
○ Change in sleep
○ Being overwhelmed or out of control
○ Physical symptoms
• Prevalence rates range from 1-8% of women
• Heritability of premenstrual symptoms 30-80%
• History of interpersonal trauma may increase risk of PMDD
• Prevalence of non-fatal suicidal behaviours increased in a graded fashion according to PMDD status
• Treatment
○ SSRIs, hormones, CBT

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66
Q

What is the genetic aetiology of depressive disorders?

A

○ Heritability of unipolar depression: 40-70%
○ First degree relatives of depressed individuals have risk of 5-25%
○ Not just presence of genes but actually the way in which the genes express themselevs
§ Diathesis and environmental factors

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67
Q

What is the neurobiological aetiology of depressive disorders?

A

○ A number of neural regions are implicated (including hippocampus)
○ There are suggestions of alterations to dopamine, serotonin, and noradrenaline

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68
Q

What is the immune aetiology of depressive disorders?

A

○ Some forms of depression may be related to immune activity
○ Suggestions that inflammation of the brain may account for some episodes of depression in some people
○ Enhancing inflammatory response leads to depressive-like symptoms
○ Anti-inflammatory medications may be helpful
○ This may only be a subset of cases

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69
Q

What is the stress aetiology of depressive disorders?

A

○ Stressors are 2.5 times more likely in depressed patients
○ 80% of MDEs preceded by major life event
○ Stress leads to more stress (helplessness/hopelessness)

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70
Q

What is the personality aetiology of depressive disorders?

A

○ Neuroticism linked to depression (and anxiety)
○ Introversion linked to depression
○ Negative self-esteem/poor self-scheme linked to depression
○ Interpersonal sensitivity may be a risk factor

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71
Q

What is the cognition aetiology of depressive disorders?

A

○ The way we think about things can influence the way we feel about them and how we behave
○ There can be a trigger (antecedent event), which leads to a belief/thought, which leads to behaviour
§ ABC model
○ Negative triad
§ People have negative views about the world, themselves, and the future
§ This pattern is particularly probelmatic in a lot of people with depression and can be helped by cognitive therapy in particular
○ Dissogenic schemas
§ Depressive thinking/styles of thought
§ Fear of losing control
§ Fear of abandonment
§ Feeling like you’re undesirable
§ Feeling incompetent
§ Feeling deserved to be punished
§ Perfectionism

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72
Q

Describe mania

A

• Abnormally and persistently elevated, expansive or irritable mood
• Expansive quality of mood characterised by unceasing and indiscriminate enthusiasm for interpersonal, sexual, or occupation interactions
• Inflated self esteem (ranging from uncritical self-confidence to delusional intensity grandiosity)
• Decreased need for sleep
• Pressured speech
• Racing thoughts
• Distractability
• Increased goal-oriented activities
• Psychomotor agitation
• Diagnosing mania
○ A distinct period of abnormally and persistently elevated, expansive or irritable mood, lasting at least 1 week (or any duration if hospitalisation necessary)
○ During the period of abnormailty, 3 or more of the following symptoms have persisted (4 if mood is only irritable) and have been present to a significant degree
§ Impaired regard for consequences
§ Agitated, excessively goal-directed
§ Flight of ideas
§ Distractability
§ Inflated self-esteem or gradiosity
§ Decreased need for sleep
○ The mood disturbance causes marked impairement in social or occupational functioning or necessitates hospitalisation to prevent harm to self or others, or there are psychotic features

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73
Q

What is the difference between mani and hypomania?

A

• Main difference between Bipolar I and Bipolar II is whether there is a manic episode involved
• In both you see a major depressive episode typically
• In bipolar I you see a manic episode as well, whereas Bipolar II only has hypomanic episodes
• In both, it is common for mixed features to occur
○ Someversion of mania and depression occurring at the same time
• Hypomanic episode
○ Abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting 4+ consecutive days
○ During this period, three or more of the following symptoms have been present
§ Agitated, excessively goal-directed
§ Flight of ideas
§ Distractability
§ Inflated self-esteem or gradiosity
§ Decreased need for sleep
§ More talkative than usual or pressure to keep talking
§ Excessive involvement in activities that have high potential in painful consequences

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74
Q

What are bipolar disorders?

A

• Bipolar I
○ One or more manic episodes usually (but not always) accompanied by major depressive episodes
○ Lifetime prevalence of 0.6%
• Bipolar II
○ One or more depressive episodes accompanied by at least on hypomanic episode
○ Lifetime prevalence 0.4%
• Cyclothymic disorder
○ At least 2 years of numerous periods of hypomanic and depressive symptoms that do not meet threshold for manic or depressive episodes
○ Lifetime prevalence of 2.4%
• Age of onset for all ~20 years
• Not usually a single episode (5.9%) or continuous presentation of features (17.9%)
Multiple episodes are common

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75
Q

What are the specifiers of bipolar disorders?

A
○ Mixed features
		○ Anxious distress
			§ Significnt anxiety
		○ Catatonia (unusual movement
		○ Melancholic features
		○ Atypical features
		○ Rapid cycling
			§ Very fast switches between depression and mania
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76
Q

What is the relationship between bipolar disorders and psychosis?

A

○ Australian survery
○ 89% of pp with bipolar in study experienced psychotic symptoms
○ 20.5% had experienced hallucinations
○ 85.7% had experienced delusions

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77
Q

What is the course of illness for bipolar disorders?

A

○ Distinct manic and depressive phases vs mixed phases
○ Clear restoration of functionning between episodes not uncommon
○ Some exhibit rapid cycling
§ Difficult to treat
○ If untreated, four findings are very consistently reported
§ Length of normal periods between episodes decreases
§ Length of each episode increases
§ Depressed phases become more likely
§ Suicide a major risk factor

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78
Q

What is the aetiology and treatment of bipolar disorder?

A

• Aetiology
○ Similar to that of depression
• Treatment
○ Mood stabilisers or antipsychotics are common
○ CBT also effective though not by itslef

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79
Q

What is the general background of schizophrenia and other psychotic disorders?

A
  • Low prevalence disorders

* Associated with high levels of stigmatisation and poor recognition by the general public

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80
Q

What is psychosis?

A

○ umbrella term - can refer to variety of syndromes or symptoms
○ At the disorder level, it refers to a group of disorders distinguished from one another in terms of
§ Symptom configuration (eg delusional disorder vs schizophrenia)
§ Duration (eg schizophrenia vs schizophreniform disorder)

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81
Q

In psychosis, what domains must individuals have abnormalities in at least one of?

A
§ Delusions
			§ Hallucinations
			§ Disorganised thinking (speech)
Grossly disorganised or abnormal motor behaviour (including catatonia)
			§ Negative symptoms
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82
Q

Describe delusions

A

□ Fixed beliefs that are not amenable to change in light of conflicting evidence
□ Persecutory delusions
® Most common
® Belief that one is going to be harmed, harrassed and so forth by an individual, organisation, or other group
□ Referential delusions
® Beliefs that certain gestures, commens, or environmental cues are directed at oneself
□ Grandiose delusions
® Beliefs that the individual has exceptional abilities, wealth or fame
□ Nihilistic delusions
® The conviction that a major catastrophe will occur
□ Somatic delusions
® Preoccupations regarding health and organ functions
□ Bizarre vs non bizarre
® Bizarre delusions are something that is completely implausable and not understandable to other same cultured-peers, don’t derive from ordinary experience
® Non-bizarre are not as easily able to be disconfirmed eg being surveilled by the police
□ Primary vs secondary
® Primary: formed without a prior event or pathological process linked to that delusion
® Secondary: secondary to other changes in mood, memory, or perception

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83
Q

Describe hallucinations

A

□ Percpetion-like experiences that occur without external stimulus
□ Auditory is most common, but they may occur in any sensory modality
□ Hallucinations may be a normal part of religious experience in certain cultural contexts
□ For diagnostic purposes, they need to occur in the context of clear sensoriums - can’t occur when someone is asleep/waking up
□ Not always distressing
□ A lminority of the population report experiencing hallucinations which are not distressing and therefore don’t seek assitance for them
□ Need to have insight - understand that what they’re hearing is a hallucination
□ Mere presence of hallucination is not sufficient to indicate a mental illness

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84
Q

Describe disorganised thinking/speech in psychosis

A

□ Also referred to as Formal Thought Disorder
□ Typically inferred from the individual’s speech:
® Clanging
◊ Speech pattern based on phonological association rather than semantic or syntactic
® Circumstantiality/tangentiality
◊ Speech including unnecessary or irrelevant detail
® Flight of ideas
◊ Sequence of loosely associated concepts are articulated . Sometimes rapidly changing from topic to topic
® Derailment
◊ Speech train steers off topic to unrelated things
® Incoherence
◊ Word salad
◊ Incomprehensible speech
® Pressure of speech
◊ Excessive spontaneuos speech production and rapid rate. Difficult to interrupt
□ Can be difficult to evaluate if the person making the diagnosis comes from a different linguistic background

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85
Q

Describe abnormal motor function in psychosis

A

□ May manifest itself in different ways, ranging from child-like ‘silliness’ to unpredictable agitation
□ Catatonia
® A marked decrease in reactivity to the environment
® Can range from a resistance to movement, or the individual maintaining a rigid, bizarre posture

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86
Q

Describe negative symptoms in psychosis

A

□ Reductions in some level of communication or human experience
□ Diminished emotional expressions
□ Avolition
® Decrease in motivated self-initiated purposeful activities
□ Alogia
® Diminished speech output
□ Anhedonia
® Decreased ability to experience pleasure
□ Asociality
® Lack of interest in social interactions and may be associated with avolition, but can also be a manifestation of limited opportunities for social interaction
□ Similar to symptoms of depression

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87
Q

What are the two groupings of symptoms in psychosis

A

§ Positive symptoms
□ Delusions, hallucinations, disorganised thinking
§ Negative symptoms
□ Catatonia (absence of movement)

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88
Q

Is it true that you are either psychotic or you’re not?

A

No
• Continuum of psychosis in the community
○ Psychotic sx (hallucinations and delusions) are present - at various degrees of severity
§ In about 5% of the general population who are not seeking help
§ In about 25% of people with non-psychotic common mental disorders such as anxiety and depression
§ In around 80% of patients with psychotic disorders

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89
Q

What is schizotypy?

A

○ Theoretical concept that psychotic symptoms lie on a continuum raning from normal dissociative, imaginary states that we all have, to extreme states related to diagnostic criteria
○ Model of personality type
○ Approach is in direct contrast to a categorical approach Describes four types of experiences
§ Impulsive non-conformity
□ Disposition to unstable mood and behaviour, particularly through guard to rules and social conventions
□ All of us lie on some place on a continuum of compulsive non-conformity
§ Introverted anhedonia
□ Tendency to introverted, emotionally flat, and unsocial behvaiour
□ Associated with the deficiency in the ability to feel pleasure from social and physical stimulation
§ Cognitive disorganisation
□ Akin to disorganised speech
□ Tendency for thoughts to become derailed, disorganised or tangential
□ All of us somewhat experience this
□ Not a fixed position - can experience this more sometimes than others
§ Unusual experiences
□ Disposition to have unusual perception, hallucinations, magical beliefs
○ Schizotypy often assessed using OLIFE measure (Oxford-Liverpool inventory of feelings and experiences)

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90
Q

What is brief psychotic disorder?

A

○ Presence of one or more of the following symptoms (at least one of these must be the first, second or third options):
§ Delusions
§ Hallucinations
§ Disorganised speech
§ Grossly disorganised or catatonic behaviour
○ Duration of an episode of the disturbance is at least 1 day but less than 1 month, with eventual full return to premorbid level of functioning
○ The disturbance is not better explained by major depressive or bipolar disorder with psychotic features or another psychotic disorder such as schizophrenia or catatonia, and is not attributable to the physiological effects of a substance or another medical condition
○ Specifiy if
§ With marked stressors (brief reactive psychosis): If symptoms occur in response to events that, singly or together would be markedly stressful to anyone in similar circumstances in the individual’s culture
§ Without marked stressors: If symptoms do not occur in response to events that, singly or together, would be markedly stressful to almost anyone in similar circumstances in the individual’s culture
§ With postpartum onset: if onset during pregnancy or within 4 weeks postpartum

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91
Q

How is delusional disorder characterised?

A

Characterised by the presence of one (or more) delusions with a duration of 1 month or longer

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92
Q

Describe schizophreniform disorder

A

○ Two (or more) of the following, each present for a significant portion of time during a one month period (or less if successfully treated). At least one must be one of the first three
§ Delusions
§ Hallucinations
§ Disorganised speech
§ Grossly disorganised or catatonic behaviour
§ Negative symptoms
○ An episode of the disorder lasts at least 1 month but less than 6 months. When the diagnosis must be made without waiting for recovery, it should be qualified as ‘provisional’
○ Approximately 1/3 of those diagnosed recover, but the remaining 2/3 progress to schizophrenia or schizoaffective disorder

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93
Q

What are the diagnostic criterion for schizophrenia?

A

○ A: Two (or more) of the following, each present for a significant portion of time during 1 month period (or less if successfully treated). At least one must be one of the first three
§ Delusions
§ Hallucinations
§ Disorganised speech
§ Grossly disorganised or catatonic behaviour
§ Negative symptoms
○ B: For a significant portion of the time since onset, the level of functioning in one or more major areas is markedly lower than prior to the onset
○ C: Continuous signs of the disturbance persist for a least 6 months
○ D: The disturbance is not attributable to the physiological effects of a substance or another medical condition

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94
Q

What is schizoaffective disorder?

A

○ An uninterrupted period of illness during which there is a major mood episode (major depressive or manic) concurrent with criterion A of schizophrenia
○ Delusions or hallucinations for 2 or more weeks in the absence of a major mood episode during the lifetime duration of the illness
○ Symptoms that meet criteria for a major mood episode are present for the majority of the total duration of the active and residual portions of illness
○ The disturbance is not attributable to the effects of a substance or other medical condition
similar to bipolar, but any time a manic episode occurs with psychosis, it is schizoaffective, not bipolar

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95
Q

Explain the details of schizophrenia

A

• Typically begins in early adulthood: 15-25
• Males tend to develop it slightly earlier than females (males between 16 and 25)
• Incidents in women is noticeably higher after age of 30
• Later onset in women could be associated with hormonal changes around menopause
• Av age of onset
○ Men: 18
○ Women: 25
• Onset under the age of 10 or over 40 is quite rare
• Lifetime prevalence of schizophrenia is 1-2%, delusional disorder is 0.2% and schiozaffective is 0.3%
• Higher prevalence amongst migrants, developing countries and 2-fold risk urban vs rural dwellers
• Approximately 1:1 male:female ratio, although McGrath suggested 3:2
• Associated features
○ Depression
○ Suicide (5-10% of people with sz commit suicide)
○ Anxiety
○ PTSD - trauma may be the experience of psychosis itself or associated with treatment (eg seclusion, restraint)
○ Substance use problems
○ Poor quality of life in general - occupational, relationship, social and emotional functioning
○ Stigma
○ Shorter lifespans

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96
Q

What is the link between psychosis and violence?

A

○ The vast majority of people with psychosis are not violent and do not display violent or dangerous behaviours
○ The vast majority of people experiencing psychosis withdraw from others when they become unwell
○ The origins of violence/aggression and psychosis are hetergenous - but factrs that may increase risk of violence/aggressive behaviour by individuals with psychotic disorders include
§ Past history of violence
§ Certain personality traits
§ Social circumstances
§ Content of auditory hallucinations
§ Substance use
§ Paranoid beliefs
§ Being male
§ Being young
○ The risk of an individual with a psychotic disorder becoming a victim of violence is up to 14 times higher than the rate of being a perpetrator
○ Yet, most studies focus on the perpetrators of violence rather than victims
○ Also, im media, stories about violent acts perpetrated by people with psychotic disorders far outweigh stories that are more sympathetic about disorder, or indicate that people with psychotic disorders are victims

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97
Q

What are the historical conceptions of schizophrenia?

A

○ Benedict Augustine Morel 1860 - demence precoce
§ The first attempt at a rigorous description of what we now know as schizophrenia
§ Based on observations of individuals displaying a set of symptoms and experiencing early onset and deteriorating course
○ Emil Kraepelin 1898- dementia praecox
§ A refined more formal definition
§ Emphasised early onset and deteriorating course
§ Differentiated from manic-depressive psychosis and other psychotic illnesses based on clusters of symptoms, onset, course, and outcome
□ Created first early ideas around different diagnoses of different psychotic illnesses
§ Symptoms emphasised were hallucinations, delusions, negativism, attentional difficulties, stereotypes, and emotional dysfunction
§ Dimentia praecox means senility of the young
□ Referencing early onset
○ Eugen Bleuler 1911 - schizophrenia
§ Conceptualised manic depression and schizophrenia on a continuum
§ Identifies that schizophrenia and bipolar were not always characterised by early onset or deteriorating course
§ His conceptualisation was adopted around the world
§ ‘Breaking the associative threads’ loosening of connections between thought structures seen as the core of the disorder
§ Primary symptoms: five ‘A’s
□ Disturbances in thinking
□ Disturbance in affect
□ Ambivalence
□ Autism
□ Avolition
○ Kurt Schneider 1959
§ Emphasised symptoms specific to schizophrenia - first rank sx (symptoms)
□ Hearing one’s voice out loud
□ Hallucinate voices talking about them
□ hallucinations in the form of running commentary
□ Somatic hallucinations produced by external agencies
□ Thought withdrawal
□ Thought insertion
□ Thought broadcasting
□ Delusional perception (ideas of reference)
□ Made feelings
□ Made actions
□ Made impulses
§ Issues with Schneiderian first rank symptoms - not specific to schizophrenia
□ But still impacted the development and refinement of diagnostic criteria in texts such as DSM
○ US-UK Cross-National Project (1972) and WHO multi-centre collaborative study (1974)
§ Varying rates of schizophrenia between countries due to lack of standardised criteria
○ Late 1970s
§ Development of the Feighner criteria and Research Diagnostic Criteria - precursors to the landmark and expansive DSM-III
□ Primarily for affective disorders, such as depression, but also for schizophrenia, anxiety and neurosis, antisocial personality disorder, and also homosexuality (which was seen as a mental illness)
○ 1980: DSM-III diagnostic criteria for schizophrenia was published
§ Narrow (neo-Kraepelinian view)
§ Changed the way diagnostic criteria were depicted
□ Developed inclusion and exclusion rules, and duration criteria
§ Included that the experience of symptms interferes with life functioning
§ Five subtypes of schizophrenia were identified
□ Paranoid
□ Disorganised catatonia
□ Undifferentiated
□ Residual
○ McGorry (late 1980s-present)
§ Realised that Kraepelin’s writing was based on an asylum setting - focused on chronic samples
§ There was an over-focus of chronic samples who are only representative of very poor outcome patients and are contaminated by institutionalisation, medication side-effects etc
§ Realised the need to prospectively study first-episode patients and prodromal (in the developing phases) patients
§ Diagnosis is not stable in first episode
○ Richard Bentall (1990s-present)
Need to study psychotic symptoms individually, not schizophrenia as a construct

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98
Q

What are the findings of family studies on psychotic disorders?

A

○ Risk of developing sz increases as a degree of genetic relatedness increases:
§ Spouse: 1% (no genetic relationship, population rate)
§ Grandchild: 2.8%
§ Sibling: 7.3%
§ One parent: 9.4%
§ Both parents: 46.3%
§ Identical twin: 45-50%
□ They share exactly their genetic makeup, and the concordance rates in not 100% - suggests there is something else going on beyond just genetics

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99
Q

What are the findings of adoption studies on psychotic disorders?

A

○ Higher concordance rates among adopted children who had one biological parent with disorder than adopted children with no affected biological relatives

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100
Q

What are the findings of epigentics studies on psychotic disorders?

A

○ Used to think there was a single gene responsible
○ Now know there are many genes involved, and most likely need to understand better Gene-environment interactions
§ People with COMT gene are more at risk for developing sz than those without it if they use cannabis (heavy use only) (Caspi et al., 2005)
• Psychosis and genetics
○ Not simple
○ Approx 1000 genes are involved

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101
Q

What are the biological factors of psychotic disorders?

A

○ Neurotransmitters
§ Dopamine hypothesis
□ Excessive dopamine function in CNS
§ Other neurotransmitters proposed to have role: norepinephrine, seratonin
○ Brain structure
§ Enlarged ventricles (indicating potential loss of brain tissue)
□ Not diagnostic, because ventrical sizes vary hugely in normal population
§ Reduced grey and white matter in prefrontal cortex - particularly associated with negative symptoms
§ Hippocampal volume seems to be larger amongst normal people than people experiencing first ep of psychosis, people who are at risk of psychosis, and larger than people with chronic schizophrenia
□ Group-based differences
□ Problem: studies are conducted in samples of people who have been unwell for a long time, and on medication fo ra long time - we don’t know if the brain structure evidence occurs for the duration of the illness
○ Brain function
§ During hallucination, there is activity in the left auditiory and visual areas of the brain, but not in the frontal lobe, which is normally involved in organised thought processes
□ Not super useful for diagnostic purposes - need more longitudinal evidence
○ Neurocognition in schizophrenia
§ Deficits in sustained auditory and visual attention
§ Problematic initial processing of information into sensory memory
§ Impaired detection of relevant stimuli that are embedded in irrelevant noise
§ Problematic organisation of information in working memory
§ Executive function
§ Language - thought disorders
§ Cognitive set changing (switching)
§ IQ deteriorated
§ Psychomotor speed
§ Not specific enough though - not diagnostic
○ Social cognition
§ Emotion perception - the ability to comprehend emotional cues in a social context
§ Social perception - the ability to comprehend communicative cues in a social context - may not be emotional
□ Predictive of relapse, and poorer illness course in general
□ Useful to target this
® Hasn’t had a lot of focus - most focus on treatment has been symptom reduction, and this treatment has oftentimes come from drug companies

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102
Q

What are the psychological factors of psychotic disorders?

A

ological factors
○ Role of family
§ Schizophrenogenic mother
□ Cold, aloof, overprotective, domineering, strips child of self-esteem, stifles independence
□ Particularly a risk if father is passive
§ This was discredited
□ Mothers of individuals with schizophrenia do not, by large, fit this definition
○ Social
§ Living in urban environment
§ Migration
§ Being socially excluded
§ If you are a member of a minority groupliving in high density environment , and particularly if you use cannabis, you’re risk of developing psychosis
○ Childhood trauma
§ Significant proportion of people with psychotic disorders have experienced traumatic childhood experiences, such as sexual and physical abuse
§ Numerous published clinical case studies whose authors suggest that these traumatic experiences may play a causal role in psychosis
§ John Reid, Richard Bentall, Tony Morrison - outspoken in criticising mainstream psychiatry/psychology for ignoring the role of chilhood sexual assault and abuse
○ Stress
§ Stress vulnerability model:
□ Everyone has a vulnerability to psychosis, someone may have a higher vulnerability than others, and added stress increases chances of having a psychotic experience
□ Buffer is coping and resilience
□ Can instil hope for patients
○ Cognitive
§ Eg Morrison, Bentall, Birchwood, Garety
§ Core model - culturally unacceptable interpretations of intrusions into awareness
§ Role of appraisal is central
§ Culturally unacceptable interpretations result from faulty knowledge of self - leads to misattribution of thought to external source
§ Response serves to increase likelihood of future intrusions
□ Disturbance in mood eg anxiety
□ Physiological arousal eg lack of sleep
□ Behavioural change
□ Cognitive change
§ Model suggests that we can work with people from a psychological/cognitive behavioural point of view to challenge those appraisals and reduce the likelihood that they will experience the appraisals, or will change their behaviour
§ Movement towards cognitive treatments rather than medication

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103
Q

Explain the relationship between substance use and psychosis

A

§ Substance-induced psychosis
□ Short-term: during intoxication or withdrawal phase
□ Ie amphetamines, cocaine, hallucinogens
§ Cannabis
□ Swedish conscipt study (Andreasson et al., 1987)
□ Those who used cannabis by 18 were 2.4 times more likely to develop schizophrenia than those who had not
□ Comparison with those who had not used cannabis by 18:
□ Problems:
® Cannabis useage was only enquired about at 18 years - no further enquiry about later usage
® Other factors were also not taken into consideration
□ Zammit et al. (2002) did further 27-year follow up on original cohort
® Relationship between cannabis use and schizophrenia persisted when controlling for other factors such as other drug use, psychiatric symptoms at baseline
® Estimated that the attributable risk of cannabis use to schizophrenia was 13%
□ Have been other further studies showing consistent findings
□ Schoeler et al. 2016: cannabis use and the risk of relapse
® Prospective cohort study followed up for at least 2 years after onset of psychosis 220 patients who presented to psychiatric services in South London with first-episode psychosis
® Change in cannabis age status (eg from user to non user) and change in pattern of continues cannabis use within the first two years after onset are risk factors for relapse
® These associations were independent of the effects of other potential confounders that vary o ver time, such as medication adherence and other illicit drug use
® The longer the period of continued (monthly) cannabis use after onset of psychosis, the more likely a patient is to experience relapse
® Cannabis use status and pattern of continued cannabis use after onset of psychosis are predicitive of subsequent relapse but not vice versa

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104
Q

What are the relapse rates of people with psychotic disorders?

A

○ Up to 80% of FEP (first-episode psychosis) patients will experience a psychotic relapse within 5 years of remission from the initial episode
○ EPPIC 7 year follow-up study
§ Symptomatic remission 37-59% of cohort
§ Social/vocational recovery: 31%
§ ~25% both social/vocational recovery and symptom remission
• Risk factors for relapse
○ Yes:
§ Substance use, medication non-adherence, carer critical comments, poor premorbid adjustment showed a consistently positive association with relapse
○ No:
§ Duration of illness, duration of positive symptoms, positive, negative, affective symptoms, age of onset, insight, gender , marital status, education, and employment

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105
Q

Explain Camberwell’s study looking into emotional expression and psychotic disorders

A

○ Brown 1950’s and 1960’s noticed many relapsing patients shared common family environments - conflict, criticism, hostile, over-involved
○ Developed Camberwell Family interview to assess patterns of family interaction
○ Relapse at 9 months and 2 years associated with:
§ High EE (expressed emotion)
§ More than 35 hours face to face with high EE family
§ Not taking neuroleptics

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106
Q

What are the potential impacts of relapse/chronic illnesses in psychotic disorders?

A
○ Unemployment
		○ Housing difficulties
		○ Poor physical health
		○ Side-effects of anti-psychotic medication
		○ Neglect of children
		○ Premature death
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107
Q

Describe the relationship between psychosis and hospitalisation/treatment

A

• Psychosis and hospitalisation
○ In Australia, preference is to treat people as outpatients, so people who are admitted to hospitals are those with more complex presentations
• Treatment
○ Pharmacological treatment - primary approach in acute phase of illness
○ Best practice: low dosage approach
○ ‘Atypical anti-psychotics’ fewer side effects than ‘typicals’
○ Soteria model
§ Highly supportive care, usually medication free, living in a community
§ Comparable results to treatment as usual
• Psychotic treatment
○ CBT - addressing hallucinations, delusions, negative symptoms
○ Substance use
○ Family education
○ Psychoeducation of patient
○ Relapse prevention
○ Occupational and social functioning

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108
Q

What are some ongoing issues with psychotic disorders?

A

• Ongoing issues
○ No biological markers or physiological tests to diagnose schizophrenia
○ Aetiology continues to be uncertain
○ No clear evidence that the concept of schizophrenia is a valid construct
○ Contiuum vs categorical models
○ Emphasis of hallucinations and delusions in diagnositc criteria
○ Accurate idenitification and treatment in prodromal or ‘ultra high risk (UHR)’ phase
○ What is the meaning of positive symptoms for the person’s self - that is their self-evaluation? Is the content important or irrelevant? What purpose do they serve?

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109
Q

What are somatic symptom disorders?

A
  • Share a common feature: the prominence of somatic symptoms associated with significant distress and impairment
    • Mental disorders that take the form of physical disorders
    • Overlap between mind and body
    • Individuals present with prominent somatic symptoms for which there is no explanation
    • People are commonly seen in primary care (GPs) or other medical settings, less commonly in psychiatric or more general mental health settings
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110
Q

What are dissociative disorders?

A

• Dissociative disorders are chractrised by a disruption of and/or discontinuity in the normal integration of consciousness, memory, identity, emotion, perception, body representation, motor control, and behaviour. Dissociative symptoms can potentially disrupt every area of psychological functioning

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111
Q

Why consider somatic symptom and dissociative disorders together?

A

• It is thought that there may be a common mechanisim underlying these disorders - specifically a dissociation or disconnect between mental awareness and another part of the usually integrated mental system
○ Somatic symptom disorders - the part of mental function that is ‘split off’ involves the sensory or motor system and affects physical functioning
○ Dissociative disorders - higher mental functions such as memory or identity are ‘split off’

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112
Q

What is the history of somatic symptom disorders?

A

○ Ancient egyptians (Kahun Medical Papyrus - 1900 BC) and hippocrates - hysteria - non-fatal bodily symptoms experienced by women (thought to be result of a wandering uterus)
○ 17th century - hypochondriasis
§ Males also
§ Relates to the experiences of medical or physical symptoms without any medical cause
○ 19th century - Briquet, Charcot, Janet
§ Wrote descriptions of people experiencing these types of difficulties
§ Anna O - first case of psychoanalysis (Freud/Breuer)
□ Father was chronically unwell - she nursed him through his illness and his death
□ Over that time, she herself became bedridden at times, developed double vision, headaches, neck weakness, loss of sensation in arms and legs, became mute at one point, disturbed speech, erratic moods, range of non-specific symptoms
□ Breuer and Freud coined the term ‘conversion’
® Her symptoms were a direct expression of her distress in being with her father
® Conversion: transformation of psychical [mental] excitationinto chronic somatic symptoms
§ In DSM-III, clear attempt to move away from psychodynamic and psychoanalytic descriptions of the disorders, but this part of the DSM retains these links
§ Briquet’s syndrome
□ Based on 430 cases who had multiple physical symptoms with no known medical rationale for developing them
§ Charcot experimented with hypnosis in treating hysteria
□ Freud worked with
§ Janet continued this work
□ Interpreted physical symptoms as being a direct representation of traumatic events through bodily memory
§ Freud initially believed that hysteria was caused by early sexual experiences - early child abuse
□ Seduction theory
□ Later discarded this theory - found that the experiences weren’t realy but were imagined

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113
Q

What is the aetiology of somatic symptom disorders?

A

○ Biological
§ Hypothalamic-Pituitary-Adrenal axis involvement?
§ Neurobiological factors
§ Gate-control theory (a model of pain)
○ Trauma
§ Individuals with somatic symptom disorders more likely than medical patients or health controls to have experienced adverse events in childhood
§ Van der Kolk - memory of trauma is not stored in declarative memory but in emotions and bodily sensations (controversial)
○ Family factors
§ Learned illness behaviour
○ Environmental factors during adulthood reinforcing illness behaviour (secondary gain)
§ Attention etc

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114
Q

What are the general cognitive factors of somatic symptom disorders?

A

○ Tendency to experience symptoms as intense and distressing (somatosensory amplification)
○ More sensitive to physical sensations
○ Selective attention to bodily sensations
○ More likely to attribute cause of physical symptoms to physical cause (rather than situational or psychological)
○ Abnormal illness behaviour - seeking treatment, tests etc
○ Vicious cycle: treatment seeking heightens anxiety which heightens physical symptoms and vigilance for symptoms, new symptoms noted, anxiety increases etc

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115
Q

What is the impact of somatic symptom disorders?

A

○ Huge levels of disability
○ Costs to the community in terms of days off work/incapacity to work
○ Compensation seeking
○ Problems for family members eg separation of children from afflicted parent is often difficult given the become care providers for the patient-patient. Secondary consequences - missed schooling, reduction of social opportunities for children
○ Burden on health care system

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116
Q

What is somatisation?

A

• Process underlying all of somatic disorders
• Distress is experienced as physical symptoms or altered bodily function
• Not necessarily ‘abnormal’ - despite DSM assuming a clear demarcation between normal and abnormal
○ Possibly used as a coping process
• Sometimes difficult to distinguish between physical disorder and somatoform disorder - questions used to try and distinguish between them:
○ How many physical symptoms are being described and for how long?
○ What degree of bodily preoccupation is there?
○ How intensely does the individual worry about their health and illness?
○ How forcefully do they seek health care?
○ Is there any history of disgruntlement with the health care system?
• Sometimes difficult to distinguish these disorders from other psychological conditions
○ Heart palpitations and upset stomach - not uncommon in relation to anxiety
○ Fatigue - not uncommon in depression
○ Vomiting and weight change - not uncommon in eating disorders
• Western countries - somatisation is viewed as abnormal
• Some Eastern countries - soatisation is viewed as the norm, expressing psychological distress is abnormal
• Physical illnesses of unknown origin - highlight the ongoing debate about mind-body split
○ Western countries: chronic fatigue, IBS
○ China: Shenjing shuairuo
○ Korea: Hwa-byung

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117
Q

What are some DSM-V characteristics of somatic symptom disorders?

A

• Suffering is authentic regardless of whether it is medically explained
• Can have these symptoms as well as having a legitimate diagnosed medical condition
○ They are not mutually exclusive

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118
Q

What are some associated features of somatic symptom disorder?

A

○ High levels of medical care - rarely alleviate’s the individual’s concerns
○ Cogntive features include:
§ Attention on somatic symptoms
§ Attribution of normal bodily sensations to physical illness (possibly with catastrophic interpretations)
§ Worry about illness
§ Fear that any physical activity may damage the body
§ Denial of psychological factors
○ Behavioural features may include
§ Repeated bodily checking for abnormalities
§ Repeated seeking of medical help and reassurance,
§ Avoidance of physical activity
○ High comorbidity with depression and increased suicide risk
○ Persistent somatic symptoms are associated with:
§ Being female
§ Older age
§ Fewer years of education
§ Lower socioeconomic status
§ Being unemployed
§ A reported history of sexual abuse or other childhood adversity
§ Concurrent chronic physical illness or psychiatric disorder (depression, anxietyy, persistent depressive disorder, panic)
§ Social stress
§ Reinforcing social factors such as illness benefits

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119
Q

What is illness anxiety disorder?

A
  • A preoccupation pattern with having or acquiring a physical illness
    • Easily alarmed by hearing about illness
    • Do not respond to appropriate medical reassurance, negative dianostic tests or benign course
    • Attempts by doctors to reassure do not generally alleviate the individual’s concerns and may heighten them
    • Illness concerns assume a prominent place in the individual’s life, affecting daily activities, and may even result in invalidism
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120
Q

What is the difference between Illness Anxiety Disorder and panic disorder/agoraphobia?

A

○ Illness anxiety
§ Aniticipated harm is less imminent than in panic - individual has time to prevent anticipated disaster by seeking medical attention
§ Concerned about lumps and bumps/blemishes
§ Health anxiety fears are persistent and enduring, may experience panic attacks triggered by illness concerns
○ Panic
§ Misinterpretations of bodily sensation –> avoidance of situations which are likely to trigger PA
§ Avoidance is an attempt to cope with or avert catastrophe
§ Misinterpret signs of anxiey
§ May be concerned panic attacks reflect a medical illness, but anixety is acute and episodic

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121
Q

What are the cognitive and psychological aspects of Illness Anxiety Disorder?

A

○ Hypersensitivity to bodily sensations
○ Heightened focus on bodily sensations
○ Heightened anxiety regarding health/illness
○ Biased thinking about threat or reality of serious disease
○ Excessive reassurance seeking
○ More distrust of medical opinion BUT higher rates of help-seeking
○ Childhood learning experiences of illness behaviour
○ Catastrophic interpretations of benign signs
○ Optimistic bias towards making judgements about own health risk

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122
Q

What is the treatment of Illness Anxiety Disorder?

A

○ Challenges
§ Helping the client feel understood
§ Arriving at a position where the client can consider alternative explanations such as
□ Possible non-catastrophic psychological alternative explanations for their problems
□ The suggested treatment rationale and strategies that flow from it

123
Q

What is conversion disorder?

A

• Classic type of somatiform disorder
• Focused on motor and sensory function
• No medical explanation for the physical symptoms they are presenting
• Some people can present unconcerned about their physical symptoms
○ Labelle en deflonce
○ Not universal though
• Can co-occur with someone who has a medical diagnosis
• Most cases don’t last long

124
Q

What are the associated features of conversion disorder?

A

○ Recent stressful event/lifechange - majority of cases
○ Familial history - similar presentation within the family network
§ Learned response to stress and trauma
○ Lower education/economic status
○ Location of residence
○ Age - uncommon in early childhood or after 35 years
○ Maintenance factors (fators that can lead to a reoccurrence of the illness)
§ Reduction in anxiety (primary)
§ Elicited caregiving (secondary)

125
Q

What are some examples of Conversion disorder?

A

○ Soldiers during wartime
○ DSM5 casebook example
§ 32 y/o woman
§ No previous neurological history
§ Began experiencing seizures with no explanation
§ Background of recently commencing uni studies
□ Thought to be a catalyst
○ Mass psychogenic disorder (mass hysteria)

126
Q

What is factitious disorder?

A

Can be done to self or done to others
Not done for monetary gain
○ Malingering
§ Individual has an identifiable, external incentive for deliberately feigning symptoms
§ NOT a mental disorder - a form of deception
• Judgement about intentionality is made by direct evidence and by excluding other causes of the symptoms - malingering goal is obvious
○ Diagnosis is through exclusion
• Person is dramatic but details are vague and inconsistent - may have extensive knowledge of medical routines - disappear/discharge when confronted
• Person may undergo multiple investigations and they are wide travellers
• Possible childhood trauma
-making up illness

127
Q

What are dissociative disorders?

A
  • Characterised by disruption of and/or discontinuity in the normal integration of consciousness memory, identity, emotion, perception, body representation, motor control, and behaviour
    • Can disrupt potentially every area of psychological functioning
    • Common in people with PTSD
    • Can also e normal experiences eg daydreaming
    • Controversial diagnoses
128
Q

What are dissociative symptoms?

A

○ Unbidden intrusions into awareness and behaviour, with accompanying losses of continuity in subjective experience (ie positive dissociative symptoms such as fragmentation of identity, depersonalisation, and derealisation) and/or
○ Inability to access information or to control mental functions that normally are readily amenable to access or control (ie negative dissociative symptoms such as amnesia)

129
Q

What is the dissociative experiences scale?

A

○ Amnesia
§ The experience of finding themselves in a place and not knowing how they got there
§ The experience of finding new things amongst their belongings that they do not remember buying
○ Depersonalisation/derealisation
§ Sometimes the experience of feeling as thought they are standing next to themselves/watching themselves do something as if they were looking at another person
§ Feeling that other people, objects etc are not real
○ Absorption
§ Staring off into space, thinking of nothing and not aware of the passage of time
§ Becoming so involved in a fantasy or daydream that it feels as though it were really happening

130
Q

What is dissociative identity disorder?

A

• Used to be known as multiple personality disorder
• At least 2 distinct personalities that switch
○ 1 host personality
○ 1 or more alters
○ Host/alters may or may not be aware of each other
• Alters may differ in many ways
○ Usually relatively uninhibited, often child-like
May have different allergies, optical prescriptions, handwriting

131
Q

What is the aetiology of dissociative identity disorder?

A

○ Sever childhood trauma is a primary risk factor
§ Vast majority of sufferers of DID report history of childhood sexual assault
§ Dissociative symptoms in general associated with trauma
§ Vast majority of individuals with DID also have PTSD

132
Q

What is the trauma theory of dissociative identity disorder?

A

○ Dissociation into different alters is a defense mechanism in which consciousness is split during traumatic stress
§ Dissociation = compartmentalisation
○ People become skilled in this defense and construct alter personalities to deal with the complexities of experience

133
Q

Describe the development/course of dissociative identity disorder

A

○ Psychological decompensation and overt changes may be triggered by
§ Removal from the traumatising situation
§ Individual’s children reaching the same age at which the individual was abused/traumatised
§ Later traumatic experiences, even seemingly inconsequential ones, like a minor motor vehicle accident
§ The death of/onset of a fatal illness in their abusers

134
Q

What is the prevalence of dissociative identity disorder?

A

○ 1957
§ Eve
§ Only recognised case in the world
§ Two alters
○ 1980 approx 200 cases internationally
○ More recently ~ 1% of whole population has DID
§ This increase could be because of past misdiagnoses
§ Or increased recognition
○ Large scale population based studies required

135
Q

What are some reasons for the controversy surrounding dissociative identity disorder?

A

○ The disorder offends our sense of self-continuity and coherence
○ Apparent explosions in cases since first case in 1957
○ Geographic focus on the USA
○ Dramatic theatrical quality of some patients
○ Alterations in symptoms
§ Animal alters, increases in average number of alters

136
Q

What is the Iatrogenic/sociocognitive theory of DID?

A

○ Psychotherapists play a role in the development of the condition by suggesting the possibility of multiple identities and legitimising it, creating the symptomology through hynosis, then shaping the patient’s behaviour through differential reinforcement
• Presentation of cases such as Eve in the media has also legitiised the disorder and taught people how to act

137
Q

What is dissociative amnesia?

A

○ Subtypes
§ Localised amnesia
□ Failure to recall events during a circumscribed period of time
□ May bebroader than amnesia for a single traumatic event (eg months or years associated with child abuse or intense combat)
§ Selective amnesia
□ Can recall some, but not all, of the events during a circumscribed period of time
§ Systematised amnesia
□ Loses memory for a specific category of information (ag all memories relating to one’s family, or childhood sexual abuse)
§ Continuous amnesia
□ Individual forgets each new event as it occurs
§ Generalised amnesia
□ A complete loss of memory for one’s life history. Can include the loss of
® Personal identity
® Semantic knowledge (knowledge about the world)
® Procedural knowledge (can no longer access well-learned skills)

138
Q

What are the associated features of dissociative amnesia?

A
§ History of trauma common
			§ Difficulty forming and maintaining relationships
			§ Dissociative flashbacks common
			§ Suicidality/self-harm common
			§ Depression common
			§ High levels of hypnotisability
139
Q

What is the epidemiology of dissociative amnesia?

A

§ 12-month prevalence among adults in US community study was 1.8% (1% for males, 2.6% for females)

140
Q

What is the course of dissociative amnesia?

A

§ Onset of generalised amnesia is usually sudden
§ Less is known about the onset of localised and selective amnesias because these amnesias are seldom evident, even to the individual
§ Individuals may reprt multiple episodes of dissociative amnesia and a single episode may predispose to future episodes
§ In between episodes of amnesia , the individual may or may not appear to be acutely symptomatic
§ Has been observed in young children, adole
§ scents, and adults

141
Q

What is the aetiology of depersonalisation/derealisation

A

§ Substantial proportion of sufferers have history of childhood interpersonal trauma but association is not prevalent or as extreme in the nature of traumas as in other dissociative disorders, such as dissociative identity disorder
§ Common proximal precipitants of the disorder are severe stress (interpersonal, financial, occupational), depression, anxiety (esp panic attacks) and illicit drug use
○ Mean age of onset is 16
○ Duration can range from a couple of hours to weeks/months
○ Associated features
§ Fear of going crazy
§ Fear of brain damage
§ Subjectively altered sensation of time (too fast or too slow)
§ Lightheadedness
§ Extreme rumination or obsessional preoccupation (do I really exist?)
§ Anxiety and depression

142
Q

Define normal eating

A

• Don’t really know what normal eating is
• Some definitions
○ Eating when you’re hungry and stopping when you’re satisfied
○ Eating because it feels good
○ Eating is only one important area in your life
○ Use moderate constraint without being too restrictive
○ Over eating at times or wishing you’d had more

143
Q

What are some types of eating disorders?

A

○ Anorexia Nervosa (AN)*
○ Bulimia nervosa (BN)*
○ Binge eating disorder (BED)*
○ Other specified feeding and eating disorder (OSFED)
○ Other unspecified feeding and eating disorder

144
Q

What are some types of feeding disorders?

A

○ Pica
○ Rumination disorder
○ Avoidant/restrictive food intake disorder
○ * = three threshold eating disorders

145
Q

What are the diagnostic criteria for anorexia nervosa?

A

○ Persistent restriction of energy intake leading to low body weight
○ Person has to have intense fear of weight gain or persistent behaviour that interferes with weight gain
○ Disturbance in how weight/shape is perceived, undue influence of weight/shape on self-evaluation, or lack of recognition of seriousness of current low weight
might say they binge eat - but it is subjective not objective

146
Q

What are some subtypes of anorexia nervosa?

A

○ Restricting (AN-R)
§ Restrict all types of calories, and do not eat much during the day
§ Does obsessive exercise
○ Binge eating/purging type (AN-BP)
§ Try to restrict food, but come to a moment where they are so hungry they binge on high caloric foods and compensate by vomiting/using laxitives
§ Also underweight
§ If they weren’t underweight they would classify as bulimic

147
Q

What is the prevalence of anorexia nervosa?

A

• Sex ratio: 10 females : 1male
○ Could reflect that males are less likely to seek help with this
• 12 month Prevalence: 0.4-0.8%
• Onset: Adolescence to early 20s
○ Younger age of onset generally has better outcome chances

148
Q

Describe the varied course of AN

A

○ Could have recovery after one episode
○ Could have fluctuation between weight restoration and relapse
○ Could have chronic course over many years
○ Could have crossover to other eating disorders (espc. BN)

149
Q

What is the comorbidity with AN

A

○ Depression and anxiety (30-60%)

○ OCD

150
Q

What were the changes from DSM-IV to DSM-V for AN?

A

○ DSM-IV used to have a ‘loss of menstruation’ criterion, and a ‘low BMI’ criterion - removed from DSM-V
○ DSM-V now has included ‘severity index’

151
Q

What are the psychological factors of AN?

A

○ Perfectionism
○ Harm avoidance
○ Feelings of ineffectiveness
○ Inflexible thinking
○ Overly restrained emotional expression
○ Some overlap with Autism spectrum disorder
○ Socially inhibited

152
Q

Describe the clinical presentation of AN

A
○ Gradual elimination of food
		○ Food rituals
		○ Preoccupation with food
		○ Ignoring hunger cues
		○ Baggy clothes to hide body
		○ Body checking
	• AN-BP psychological factors more similar to bulimia nervosa
		○ Presents with higher substance use disorders
153
Q

What are the health and cognitive complications of AN

A

○ Cardiac, endocrine (incl. osteoporosis, amenhorrea), gastro-intestinal etc
○ Frequent hospitalisation common
○ Highest death rate of any mental health condition
• Cognitive changes
○ Mild deficits in executive functioning, memory, verbal, and visuospatial processing
○ Can impede recovery - eg rigid thinking
§ Doesn’t go away very easily
§ Endophenotype - something that can be seen before, during, and after illness
○ Mostly improves with weight restoration
○ Cog + health issues can severely impact adolescent development
• Less likely to want to talk & engage - difficult for group therapy
• 23.4% of people more on to develop BN-BP
• 10.8% move into OSFED

154
Q

What is the diagnostic criterion for bulimia nervosa?

A

○ Recurrent episodes of binge eating (size of meal is larger than what normal people would eat, time - within two hour time frame & loss of control)
○ Use recurrent inappropriate, compensatory behaviour to prevent weight gain (eg purging, laxatives/diuretics, fasting, excessive exercise)
○ Occurs at least once a week for 3 months
○ Self-evaluation unduly influenced by body shape and weight
○ Does not occur exclusively during and AN episode

155
Q

What are the subtypes of bulimia nervosa?

A
○ Purging 
			§ Vomit/use laxatives/diuretics
		○ Non-purging 
			§ Fasting and excessive exercise
	•  *DSM-V reduced the frequency threshold because there were too may atypical eating disorders (OSFED) - tried to get more of these people into the official diagnostic criterion o f eating disorders
156
Q

What is the prevalence and onset of bulimia nervosa?

A

• Sex ration: 10 female : 1 male
• Prevalence = 1-1.5%
• Onset
○ Late adolescence/early adulthood (later than AN)
○ May be preceded by AN
○ Frequently begins during or following an episode of dieting

157
Q

What is the varied course and comorbidity of bulimia nervosa?

A

• Varied course
○ Can be chronic or intermittent
○ For many, persists for several years
§ But generally has a better outcome that AN
○ Periods of remission often alternate with recurrences of binge eating
○ Purging may become addictive
• Comorbidity
○ Depression and anxiety
○ Substance use
○ Personality disorders (eg borderline personality disorder)

158
Q

What is the clinical presentation and psychological factors of bulimia nervosa?

A

• Clinical presentation
○ Binge-purge cycle
○ Preoccupation with food
○ Recognise that the behaviour is maladaptive
○ Weight typically in the average range
• Psychological factors
○ Low self-esteem and guilt
○ Impulsivity
• If seen without personality disorders, tend to help each other out in group therapy sessions
• Approx 5.7% move on to develop AN-R

159
Q

What is binge eating disorder and what are its diagnostic criteria?

A

• Did not used to have its own diagnostic criteria but there was enough research for a specific criteria in the DSM-V
• Diagnostic criteria
○ Recurrent binge eating (objective)
○ Three or more of the following
§ Eating more rapidly than normal
§ Eating until uncomfortably full
§ Eating large amount of food when not hungry
§ Eating alone due to embarrassment or disgust
§ Depressed or guilty after over-eating
○ Marked distress regarding binge eating
○ Occurs once per week, for 3 months+
§ DSM-IV was twice per week
○ No regular use of inappropriate compensatory behaviours

160
Q

What is the prevalence, and clinical features of binge eating disorder?

A

• Prevalence
○ 12 month: 2-3%
○ Gender difference is less skewed
○ Prevalence higher in very overweight populations
• Clinical features
○ Guilt and shame regarding behvaiours
○ Eat when not hungry
○ Eat for emotional control
○ Associated with increased psychological distress and metabolic disturbance
• If seen without personality disorders, tend to help each other out in group therapy sessions

161
Q

What are the DSM-V severity indexes of eating disorders?

A

• Anorexia nervosa (BMI)
○ Mild: greater than or equal to 17
○ Moderate: 16-16.99
○ Severe: 15-15.99
○ Extreme: lower than 15
• Bulimia (frequency of weekly inappropriate compensatory behaviours)
○ Mild: 1-3
○ mODERATE: 4-7
○ Severe: 8-13
○ Extreme: more than 14
○ BED the same as BN, but only for binge eating episodes
• Problem:
○ Does not appropriately capture the severity of the patients
§ Most of the clinical samples are in the mild category which doesn’t make sense for a clinical sample
○ Not backed up by research (research is only coming out after it was created)

162
Q

What is OSFED (other specified feeding or eating disorders?

A

• Everything that doesn’t fit into the other categories
• Clinically significant distress or impairment but do not meet full criteria for other disorders
• Examples
○ Atypical AN
§ All criteria have been met, except despite significant weight loss, the individual’s weight is within or above the normal weight range
§ Similar health consequences, impairments, and comorbidities to AN
§ Harder to detect as a person does not present as underweight
○ Purging disorder
§ Recurrent purging behaviour to influence weight or shape in the absence of binge eating
§ Frequency: once per week for the past three months
§ BMI should be in normal range
§ Krug et al., 2020 cluster analyses
○ Night eating syndrome
§ Recurrent episodes of night eating
§ Eating after awakening from sleep, or by excessive food consumption after the evening meal
• 18.7% move on to having no ED

163
Q

What is UFED (unspecified feed or eating disorder)

A

• Clinically significant distress or impairment but do not meet full criteria for other disorders
○ Used when clinician chooses not to specify why criteria are not met
○ Or presentations where there may be insufficient information to make a more specific diagnosis (eg in emergency room settings
• Brings in more heterogeneity than OSFED
• Need more research on the usefulness of this

164
Q

What is avoidant restrictive food intake disorder (ARFID)?

A

• Diagnostic criteria
○ Persistent failure to meet appropriate nutritional and/or energy needs associated with one of the following
§ Significant loss of weight (or failure to achieve expected weight gain or faltering growth in children)
§ Significant nutritional deficiency
§ Dependence on enteral feeding or oral nutritional supplements
§ Marked interference with psychosocial functioning
○ Not better explained by lack of available food or by an associated culturally sanctioned practice
○ The behvaiour does not occur exclusively during the course of AN or BN, and there is no evidence of a disturbance in the way one’s body weight or shape is experienced
○ The eating disturbance is not attributed to a medical condition, or better explained by another mental health disorder
• Age of onset younger than AN/BN
• Associated with
○ Childhood picky eating
○ GAD
○ Gastrointestinal symptoms
○ Comorbid medical symptoms
○ Less likely to have a mood disorder than AN or BN
○ Slightly more common in males
• Not much research has been donw

165
Q

What is Pica?

A

• DSM Criteria
○ Persistent eating of nonfood substances for a period of at least 1 month
○ The eating of the nonfood substance is inappropriate to the developmental level of the individual
○ It is not part of a culturally supported or socially normative practice
○ If occurring in the presence of another mental disorder or during a medical condition (eg pregnancy), it is severe enough to warrant independent clinical attention
• Prevalence data yet to be established, appears to be more common in those with an intellectual disability
• Increased prevalence in pregnancy

166
Q

What is rumination disorder?

A

• Criterion
○ Repeated regurgitation of food for a period of at least one month. Regurgitated food may be re-chewed, re-swallowed, or spit out
○ The repeated regurgitation is not due to medical condition
○ Does not occur exclusively in the duration of AN/BN/BED/ARFID
○ If occuring in the presence of another mental health disorder it is severe enough to warrant independent clinical attention
○ Prevalence data yet to be established, thought to occur alongside intellectual disability

167
Q

Describe disordered eating

A
  • Subthreshold eating pathologu (not in DSM)
    • Common in adolescence (approx. 16%)
    • Associated with psychosocial impairment and comorbid pathology
    • Precursor to ED
168
Q

What is orthorexia?

A

• Not an officaly DSM category
• May start as clean eating, progresses to elimination of mnay food groups
• Inflexible eating behaviours aimed at purity
• Emotional wellbeing overly dependent on eating the ‘right’ foods
• Similarities with AN
○ Health risks/malnutrition for cutting foods
○ Rigid food rules and preoccupation with food
○ Interference in normal functioning
• Reasonably recently detected
○ Impact of media/culture on psychopathology
• When does clean eating become unhealthy
○ Impact on functioning
○ Healthy vs unhealthy food labels - black and white

169
Q

Describe Muscle dysmorphia

A

• Preoccupation about not having enough muscles
○ Genuinely see self as smaller
○ Can lead to disordered eating (more protein, less fats)
• Mostly affects males
• Not an ED but substantial body image component
○ Subtype of body dysmorphic disorder
○ ‘Bigorexia’ - comparable to AN body image disturbance

170
Q

What is the aetiology of eating disorders?

A

• Rsik factors from longitudinal cohort studies
○ Dieting - #1 risk factor
○ Personality factors
§ Neuroticism
§ Negative affect
§ Perfectionism (AN)
○ Body dissatisfaction
○ Thin-ideal internalisation and social pressure to be thin
○ Perinatal factors, including premature birth and complications during delivery
○ Parental psychiatric factors
○ Genetic factors
• Numerous correlates identified, incl. child abuse, certain family environments, weight-based criticism

171
Q

Explain the role of gender on eating disorders

A

○ Female gender is a big risk factor for Eds - but males likely underrepresented
○ Eating disorders in males
§ Average onset of ED is later than for females
§ Associated with jobs requiring a particular body look or exercise treatment
§ Muscularity more likely to be a focus
§ Dieting less common risk factor for men
§ Present with more premorbid ‘overweight’
§ 15% of gay or bisexual men have struggled with Eds, and around 42% of men with an ED identify as gay or bisexual

172
Q

What are the findings of twin studies on eating disorders

A

○ Non-shared environment (things that make the twins different eg trauma, personality, cognitive style) are the most important determinant for ED rather than shared environment (eg family)
○ Non-shared environment has greated contribution followed by genetics, followed by shared environment

173
Q

Explain the role of genetics on eating disorders

A

○ Eating disorders aggregate in families - heritability estimates 40-60%
○ Candidate gene studies (eg serotonin transporter)
§ Specific genes can contribute
○ Genome Wide Association Studies (GWAS)
§ Identified 1 significant locus on chromosome 12 - also associated with psychiatric and metabolic factors
○ Gene x environment interactions
§ Not deterministic
§ Combination of genetic susceptibility and environmental factors
§ Suggests environment is very important
§ Environment can only be problematic with certain genetic makeup

174
Q

Explain thinspiration vs fitspiration

A

• Thinspiration
○ Aimed to promote weight loss and glorify disordered eating
• Fitspiration
○ Aimed to promote healthy and fit lifestyles
○ But also idealises the extremely thin body, with additional emphasis on muscle tone - related to body dissatisfaction, negative mood and disordered eating

175
Q

Describe the experimental EMA design to assess fitspiration

A

• Experimental EMA design to assess fitspiration (Krug et al., 2021 & Yee et al., 2021)
○ Random assignment to view fitspiration or neutral image
○ Post-image ratings nased on
§ Pressure to change body image
§ Satisfaction variables
§ Disordered eating
○ Not many significant findings in females
○ Significant findings in males
§ Viewing fitspiration images led to
□ Higher body fat dissatisfaction
□ Muscularity dissatisfaction
□ Negative mood
□ Urge to engage in behaviours to reduce body fat
□ Urge to engage in behaviours to increase muscularity
§ Viewing thinspiration images led to
□ Decreased body fat dissatisfaction
□ Decreased muscularity dissatisfaction
□ Increased negative mood
□ No urge to engage in behaviours to reduce body fat
□ Increased urge to engage in behaviours to increase muscularity
§ Fitspiration images were more detrimental

176
Q

What are the aetiology models of eating disorders?

A

• Dual pathway model (DPM) of BN
○ Binge eating as a result of restriction
○ Binge eating as an emotion regulation technique
○ Empiraical evidence
§ Cross sectional studies have shown 50% variance, but unclear on the role of dietary restraint
§ Longitudinal studies account for 30-54% variance, and all hypothesised paths were supported
§ Not enough longitudinal studies
§ No real controlling for temporal stability of bulimic pathology
○ Theoretical limitation of DPM
§ Only accounts for ~54% variance which suggests other factors need considering –> personality?
§ Cannot account for why sociocultural factors only impact some people
• Tripartite Influence model for eating pathology
○ Need more longitudinal evidence
○ Doesn’t consider social media
• Transdiagnostic model of Eds (Fairburn)
○ There are weight and shape concerns which are the most important maintenance factors for any eating disorder
○ Need to focus on overevaluation of eating, shape, and weight - transdiagnostic factor
○ Also recognises other transdiagnostic factors which can contribute (eg perfectionism, low self-esteem, mood intolerance)
○ Two pathways that a clinician can take during treatment
§ One describes behaviours leading to bulimia
§ One describes behaviours leading to AN
○ Allows you to tailor treatment according to behaviours

177
Q

How do the risk factors fit together for eating disorders?

A

• How do the risk factors fit together?
○ Predisposing:
§ contributing towards a vulnerability towards ED
○ precipitating (stressors):
§ lead to weight loss and the gains associated with weight loss are discovered
○ Perpetuating
§ Maintain weight loss, trapping individual into an inescapable situation

178
Q

What are the treatment approaches and outcomes of eating disorders?

A

• Evidence-based treatment
○ Limited evidence for specific treatments
§ Family-based treatment for anorexia nervosa in adolescents
§ CBT/CBT-E and guided self-help for bulimia nervosa and binge eating
○ Early symptom improvement predictive of better outcomes long term
§ Important to get treatment quickly
○ ED research is still in its infancy - doesn’t mean that treatment doesn’t work
§ EDS unlikely to spontaneously recover without treatment
§ Can involve inpatient, day program , or weekly individual therapy
• Barriers in recovery
○ Many don’t seek treatment
§ Don’t recognise seriousness of condition
§ May be encouraged by friends/family - but they often thrive off secrecy
§ Fearful of change
§ Egosyntonic (consistent with one’s ideal self-image)
§ Very low BMI often quires inpatient admission
○ Bhevaiours become deeply ingrained
○ Evidence-based practice often involves targeting behaviours early, followed by addressing body image and related factors
• Emerging approaches
○ Health in every size movement
§ Body shape/weight is heavily genetically influenced
§ Little evidence that dieting works long term
§ Being overweight does not necessarily equate to unhealthy
○ Body positivity
§ Embracing uniqueness and diversity of bodies
§ Fighting against thin ideal

179
Q

What are types of trauma and stressor related disorders?

A

• Reactive attachment disorder
○ Pattern of disturbed and developmentally inappropriate behaviour in childhood, in which child rarely or minimally turns to an attachment figure
○ Essential feature is absent/grossly undeveloped attachment between child and caregiving adult
○ Believed to have capacity to form attachments, but because of limited opportunities during development they fail to show this occurring
○ Prevalence
§ Unknown
§ Seen very rarely in clinical settings
§ Found mostly in young children experiencing extreme neglect before being placed in institutional care
□ Occurring in less that 10% in those children
• Disinhibited social engagement disorder
○ Characterised by disturbance in attachment - individual exhibits culturally inappropriate overly familiar behaviour with strangers
○ Childhood-related disorder, but diagnosis should not be made before child is developmentally able to make decisions around care-seeking
○ Must be 9+ months for diagnosis
○ Prevalence
§ Unkown
§ Quite rare
§ Occurs amongst neglected/abused children
• Acute stress disorder
• Adjustment disorders
• Other specified trauma- and stressor- related disorders
• Unspecified trauma -and stressor- related disorder
• Post-traumatic stress disorder

180
Q

What is the history of PTSD?

A

• Wilfred Owen - Lieutenant in WW1
○ Hospitalised after surviving very traumatic circumstances under deployment
§ For ‘shell shock’
○ Wrote poem Dulce and Decorum Est (poem about ptsd)
○ Recovered, and returned to war, but then died at 25
• Many different names
• Samuel Pepe - famous diarist from 1600s wrote of his experiences of the great fire
• Charles Dickens - experiences of a railway accident
• Russian army in 1904/05 recognised something that is now recognised at PTSD
• Shell shock
○ Shell shock was recognised in WWI but was seen as a weakness
§ A character flaw
§ Only soldiers who developed WWI as a result of enemy combat was elligible for pension/wound stripe
○ Idea that shell shock would stop after they were back from the war
• Wasn’t until Vietnam war that it was better understood and recognised
○ Mainly due to lobbying by returned service people and the health insurance industry in US around the Vietnam war and follow-up period when it was recognised that many people in that war were not normal after returning
○ Originally going to be called Vietnam War syndrome in DSM-III
○ Also recognised that people experienced delay in symptom development
○ Lobbying grew until there was sufficient evidence to acknowledge that there was a syndrome
○ Also a recognition that other traumatic experiences could result in the same stress
○ Lead to broad disorder in DSM-III rather than Vietnam War disorder

181
Q

What are the DSM-V criteria for PTSD?

A

○ Apply to adults, adolescents, and children over age 6
○ A: Exposure to actual or threatened death, serious injury, or sexual violence in one or more of the following ways
§ Directly experiencing the traumatic events
§ Witnessing (in person) the event as it occurred to others
§ Learning that the traumatic event(s) occurred to a close friend or family member. In cases of actual or threatened death of a family member/friend, the event(s) must have been violent or accidental
§ Experiencing repeated or extreme exposure to aversive details of the traumatic event(s) (eg first responders collecting human remains, police officers repeatedly exposed to details of child abuse)
□ This does not apply to exposure through electronic media, television, movies, or pictures, unless this exposure is work related
® Added after 91
○ Rest of criterion forms under four major symptom cluster:
§ Re-experiencing
□ B
® Presence of one or more of the following intrusive symptoms
◊ Recurrent, involuntary, and intrusive distressing memories of traumatic events
◊ Recurrent distressing dreams in which the content and/or affect of the dream are related to the traumatic event
◊ Dissociative reactions (eg flashbacks) in which the individual feels or acts as if the traumatic event were recurring
◊ Intense or prolonged psychological distress at exposure to internal or external cues that symbolise or resemble an aspect of the traumatic event
◊ Marked physiological reactions to internal or external cues that symbolise or resemble an aspect of the traumatic event
§ Avoidance
□ C
® Persistent avoidance of stimuli associated with the traumatic event, beginning after the traumatic event occurred, as evidenced by one or more of the following:
◊ Avoidance of, or evidence to avoid distressing memories, thoughts, or feelings about or closely related to the traumatic event
◊ Avoidance of or efforts to avoid distressing memories, thoughts, or feelings about or closely related to the traumatic events
§ Negative cognitions
□ D
® Negative alterations in cognitions and mood associated with the traumatic event, beginning or worsening after the traumatic event occurred, as evidenced by two or more of the following
◊ Inability to remember an important aspect of the traumatic event (typically due to dissociative amnesia and not to other factors such as head injury, alcohol or drugs)
◊ Persistent and exaggerated negative beliefs or expectations about oneself, others, or the world
◊ Persistent distorted cognitions about the cause or consequences of the traumatic event that lead the individual to blame him/herself or others
◊ Persistent negative emotional state (beginning or worsening after experience of the event)
◊ Markedly diminished interest or participation in significant activities
◊ Feelings of detachment or estrangement from others
◊ Persistent inability to experience positive emotions
◊ *similar to depression, but if these symptoms were not present prior to the event, then the diagnosis can be PTSD
§ Arousal
□ E
® Marked alterations in arousal and reactivity associated with the traumatic event, beginning or worsening after the traumatic event occurred as evidenced by two or more of the following
◊ Irritable behaviour and angry outbursts (with little or no provocation) typically expressed as verbal physical aggression toward people or others
◊ Reckless or destructive behaviour
◊ hypervigilance
◊ Exaggerated startle response
◊ Problems with concentration
◊ Sleep disturbance
§ Duration of the disturbance (in criterion B, C, D, E) is more than 1 month
§ The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning
§ Disturbance is not attributable to the physiological effects of a substance or other medical condition
○ *Medical incidents can be considered traumatic if they are sudden and catastrophic eg waking during surgery and anaphylaxis
○ Used to be considered an anxiety disorder
○ Specify
§ Whether any dissociative symptoms
§ If with delayed expression: if the full diagnostic criteria are not met until at least 6 months after the event (although the onset and expression of some symptoms may be immediate)

182
Q

What is the panic creep of PTSD?

A

○ Number of different combinations of the various criterion described in these editions of the DSM that can result in diagnosis:
○ Leads people to wonder what we’re actually seeing here - is it really just one disorder that we’re seeing?
§ Questions of the validity of the PTSD DSM criterion
§ What does that mean for treatment, duration, and outcome of illness?

183
Q

What is acute stress disorder?

A

• Highly resembles PTSD
○ Definition for traumatic event is the same for PTSD and acute stress disorder
○ Have to experience a range of the same experiences/symptoms as PTSD (but not so many)
• Criterion
○ Exposure to traumatic event - identical to criterion A for PTSD
○ Presence of nine (or more) of the symptoms from any of the 5 categories of intrusion, negative mood, dissociation, avoidance, arousal, beginning or worsening after the traumatic event occurred
○ Duration of the disturbance (symptoms in criterion B) is 3 days to 1 month after trauma exposure
○ Disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning
○ Disturbance is not attributable to the physiological effects of a substance, or another medical condition and is not better explained by brief psychotic disorder
• Not much epidemiological evidence available
○ Because diagnosis has to happen in that acute period, and people don’t often seek help in that period unless they have been injured
§ Most evidence comes from road accident survivors, people who are admitted to trauma centres because they are already being monitored for physical injury

184
Q

What is the data and trajectory of Acute Stress Disorder?

A

• Data
○ Recent meta-analysis of road accident survivors
§ 13 studies comprising 2989 patients
§ 15.8% of patients met criteria for ASD (using DSM-IV)
• Trajectories
○ Bryant: longitudinal study of what happened to people with some trauma and met DSM-IV criteria for
§ Around 70% did not develop PTSD (resilient group
§ Around 4% have chronic course
§ Around 6% have some initial symptoms but recover
§ Around 8% are ok initially but worsen
○ Galatzer-Levy et al. study
§ Four classes:
□ Resilient - 70%
□ Group with initial stress but gradually got better - 21%
□ Group with delayed reaction - 11%
□ Chronically distressed - 9%

185
Q

What are the rates of traumatic experiences?

A

○ Men are more likely to experience traumatic events than men (65%:50%)
§ Most of these experience more than one trauma
○ Prevalence of the experience of trauma is higher in clinical populations - up to 80%
§ Suggests that there are different trajectories following trauma that the pathway of ASD and PTSD are not the only sequeli to the experience of trauma (but association does not mean causation)

186
Q

What are the types of traumatic experiences?

A

○ Most common events overall
§ Witness someone being injured or killed
§ Involved in fire/natural disaster
§ Being involved in life-threatening accident
§ All of these more likely to have been experienced by men
□ Men are more likely to have experienced some kind of physical assault/attack
□ Women are more likely to experience rape, sexual molestation, childhood parental neglect and childhood physical abuse
§ People in developing nations are much more likely to experience trauma than developed nations
□ Risk of developing PTSD varies according to the type of trauma experienced
□ Assault (sp. Sexual) are more likely to be followed by post-trauma symptoms than other traumas

187
Q

Describe PTSD epidemiology

A

○ Women are more likely to develop PTSD after a traumatic event than men (women: 20-30%, men: 8-13%)
§ Maybe explained by the PTSD likelihood according to trauma type, but not fully explained
§ Women are still 4 times more likely to experience PTSD even when the trauma is controlled for
○ Annual prevalence = 1.5-3%

188
Q

What are the risk factors for PTSD

A

○ Pre-trauma factors
§ Gender: female
§ Personality: high neuroticism
§ Age: young
§ Lower intelligence/education
§ Unstable family during childhood
□ Says something to do with attachment?
§ Pre-existing mood/anxiety disorder
§ Family history of mood/anxiety disorder
§ Biological: attenuated cortisol levels
○ Trauma-related factors
§ Type of trauma (interpersonal)
§ Perceived degree of life threat
§ Predictability and controllability
§ Duration and frequency
○ Peri-traumatic reactions (during)
§ Arousal: heart rate in acute post traumatic phase
§ Dissociation at time of trauma
○ Post-traumatic factors (we can control this)
§ Level of social support and positive support
§ Validation of the experience
§ Opportunities to process the experience

189
Q

What are the associated features of PTSD?

A
○ Anger
		○ Depression
		○ Anxiety
		○ Substance use/abuse
		○ Emotional lability 
		○ Impulsive and/or self harming behaviour
		○ Physical complaints
190
Q

What are the psychological processes of PTSD?

A

• memory
○ Contradictory pattern: bias towards vivid recall of trauma-related material or vague/error-prone memories
○ Reliving experiences of flashbacks: different to normal autobiographical memory b/c dominated by sensory detail but typically disjointed and fragmented
○ Lower levels of working memory capacity: related to capacity to prevent unwanted material from intruding and affecting performance. Working memory associated with IQ - explains lower IQ risk factor
• Dissociation
○ Mild dissociative reactions are common under stress - ie 96% of soldiers undergoing survival training
• Cognitive-affective reactions
○ DSM-IV criteria
§ Individual had to experience intense fear, helplessness, or horror at the time of the experience
○ Taken away from DSM-V because not everyone has that response
• Cognitive appraisal and emotion
○ Appraisal of the cause of, responsibility for, and future implications of trauma can result in negative emotions
○ Anger towards others and shame around the experience predict slower recovery from PTSD
○ Can influence a person’s trajectory, engagement in psychological treatment, and recovery
• Beliefs
○ General increase in negative beliefs about world, self, and others
○ Can be associated with beliefs that there has been a permanent change in oneself and one’s capacity to achieve one’s goals

191
Q

What the effects of conditioning on people experiencing PTSD?

A

• Evidence that the principles of classical conditioning operate during the development of PTSD
○ Certain cues that are present in the environment get conditioned to produce the same response that occurred during the time of trauma
○ Eg soldiers watching fireworks
○ In the case of PTSD, single-trial learning can occur
§ Maybe a survival technique - need to learn quickly because it may save our life
○ Generalisation
• Does not explain the beliefs, the memory etc

192
Q

What is the cognitive behavioural model of PTSD?

A

• Accounts for stimulus and response component
• Also acknowledges that there is much more going on at a higher level
• Dominant model for explaining PTSD
• If we can address these dysfunctional strategies, help the individual understand their negative appraisals, and help the memory processing along, we can help people with PTSD very well
○ But individual has to want to come along to therapy

193
Q

What are the barriers to treatment for PTSD?

A
  • Concerns related to stigma, shame, and rejection
    • Low metal health literacy
    • Lack of knowledge and treatment-related doubts
    • Fear of negative social consequences
    • Limited resources, time, and expenses
    • Specific trauma-related barriers to mental health service use, esp. concerns about re-experiencing the traumatic events
194
Q

What is complex ptsd?

A

• Does not appear in DSM-V
○ Felt that there was not enough evidence to include it
• Can be developed across all age groups
• Associated with chronic and repeated traumas
• Includes symptoms of PTSD
• BUT ALSO
○ The development of persistent and pervasive impairments in affective, self and relational functioning including
§ Emotion dysregulation (heightened/lacking)
§ Interpersonal dysfunction
§ Difficulties in self-identity
• These additional domains are thought to reflect the disturbance associated with chronic and repeated experience of trauma, which results in enduring and persistent and pervasive disturbance at almost personality-level

195
Q

How do we differentiate complex PTSD from PTSD?

A

• Cloitre et al (2013)
○ Latent profile analysis on assessment data from 302 treatment-seeking individuals with diverse trauma histories, ranging from single events (eg 9/11 attacks) to sustained exposures (eg childhood sexual abuse)
○ Cloitre theorised that someone with complex PTSD would have high levels in all PTSD-related symptoms/associated features
○ Theory supported
○ People argued that some of those associated features sound like borderline personality disorder - could be someone with that personality disorder who also has PTSD from some trauma
○ To address this, she included people with BPD, and measured how many people with BPD, PTSD, CPTSD, and nothing experienced PTSD, CPTSD and BPD symptoms
§ Found that CPTSD had highest levels of CPTSD symptoms and much lower BPD symptoms

196
Q

What is adjustment disorder?

A

• Criteria
○ The development of emotional or behavioural symptoms in response to an identifiable stressor occurring within 3 months of the onset of the stressor
○ These symptoms or behaviours are clinically significant, as evidenced by one or both of the following
§ Marked distress that is out of proportion to the severity or intensity of the stressor, taking into account the external context and the cultural factors that might influence symptom severity and presentation
§ Significant impairment in social, occupational, or other important areas of functioning
○ The stress-related disturbance does not meet the criteria for another mental disorder and is not merely an exacerbation of a pre-existing mental disorder
○ The symptoms do not represent normal bereavement
○ Once the stressor or its consequences have terminated, the symptoms do not persist for more than an additional 6 months
• Some people think that this disorder is pathologising of normal human experience
• There is no requirement of any specific type of symptoms that people need to experience
○ Seen as problematic
• Definition for type of stressor is very vague - problematic

197
Q

How common is adjustment disorder?

A

• Quite common
○ Almost three times more common than major depression (13.7%:5.1%) in acutely ill medical in-patients
○ Diagnosed in up to one third of cancer patients experiencing a recurrence
○ Primary care-rates varying from 1-18% people seen for mental health problems
○ Among psychiatric inpatients, 9% of consecutive admissions to an acute public sector unit were diagnosed with adjustment disorder
○ In AUS no one would be admitted with just adjustment disorder

198
Q

What are the problems with adjustment disorder?

A

○ No standardised diagnostic assessment tool
§ No validity or reliability
○ Has not been included in any of the major epidemiological studies
○ Medicalises ‘problems of living’
○ A ‘wastebucket diagnosis’ for those who fail to meet the criteria for other disorders
○ Comorbidity? Do not know much, but the few studies that have said anything have said that there is roughly 50% comorbidity with modd/anxiety disorders
○ Best practice treatment?

199
Q

What are personality disorders?

A

• Personality
○ Describes the individual differences of a person in temrs of their behaviour, emotions and thoughts
• Personality disorder
○ Longstanding, pervasive, inflexible patterns of behaviour and inner experiences that leads to distress
○ Have to be patterns of maladaptive behaviour in at least two ares
§ Cognition
§ Emotions
§ Relationships
§ Impulse control
○ Often comorbid with other DSM-V diagnoses
§ Eg, Depression, anxiety
§ More severe symptoms and poorer outcomes when comorbid
§ 50% of people with PD meet criteria of another PD

200
Q

How do we classify personality disorders?

A
• DSM-V categorical approach
	• Classifies in 3 different clusters
		○ A: Odd/eccentric
			§ Paranoid PD
			§ Schizoid PD
			§ Schizotypal PD
		○ B: dramatic/erratic
			§ Antisocial PD
			§ Borderline PD
			§ Histrionic PD
			§ Narcissitic PD
		○ C: Anxious/fearful
			§ Avoidant PD
			§ Dependent
			§ Obsessive-compulsive
	• Diagnostic reliability
		○ Initially poor, improved since DSM-III
	• Test-retest reliability
		○ 1/2 of those initially diagnosed with PD did not receive same diagnosis 1 year later
201
Q

What is the gender ratio of personality disorders?

A
• Gender bias
		○ Certain diagnoses applied more often to men, others to women
		○ Females > males for:
			§ Borderline PD
			§ Histrionic PD
			§ Dependent PD
202
Q

What is the epidemiology of personality disorders?

A
○ 6.5% of adults meet PD criteria in AUS
		○ US: 9%
		○ Norway: 13%
		○ Western countries: 12%
		○ In mental health settings: 25-40%
203
Q

What is the most common personality disorder?

A

§ In treatment settings: avoidant

§ In community: obsessive-compulsive

204
Q

What are the core features of personality disorders?

A

○ Functional inflexibility
§ Failure in adaptation to changing and varied life experiences
§ A tendency to rigidly apply a range of behavioural strategies or responses across diverse life situations even when inappropriate
○ Self-defeating behaviour patterns
§ Typical ways of responding of coping that worsen the current situation or are explicitly damaging for the person
§ Nevertheless, the person demonstrates limited capacity to intervene constructively or to learn from experience
○ Tenuous stability under stress
§ Marked instability in mood, thinking, or behaviour during difficult periods

205
Q

Describe personality disorders in the DSM

A

○ Introduced for the first time in DSM-III
§ More interest in PDs
○ Considered Axis II disorder
§ Encouraging clinicians to think of PDs as co-existing with Axis-I disorders
§ PDs as interacting with Axis-I disorders - impact presentation, treatment, adherence, response etc
§ Axis-I = clinical disorders, Axis-II = personality disorders
§ Not anymore since DSM-V removed axis system
□ Because they also introduced a form of hierarchy - placing axis I as more important

206
Q

What are the general diagnostic criteria for personality disorders?

A

○ An enduring pattern of inner experiences and behaviour that markedly deviate from the expectations of the individual’s culture. The pattern is manifested in two or more of the following
§ Cognition
§ Affectivity
§ Interpersonal functioning
§ Impulse control
○ The enduring pattern is inflexible and pervasive across a broad range of personal and social siutations
○ Leads to clinically significant distress or impairment in social, occupational, or other important areas of functioning
○ The pattern is stable and of long duration, and its onset can be traced back to at least adolescence or early adulthood
○ Not better explained as a manifestation or consequence of another disorder
○ Not due to physiological effects of substance or medical condition

207
Q

What are the three Ps of personality disorders?

A
○ Pathological
			§ Outside range of normal variation
		○ Persistent
			§ Frequently present over period of at least 5 years with onset by early adulthood
		○ Pervasive
			§ Apparent in a variety of contexts
208
Q

What are the issues with diagnosing personality disorders?

A
○ Establishing prevalence over time is difficult
		○ Age requirements are difficult
		○ Role of gender norms
		○ Impact of cultural background
		○ Diagnosis process
209
Q

Describe paranoid personality disorder

A

• Diagnositc criteria
○ Pattern of distrust and suspiciousness such that others’ motives are interpreted as malevolent
§ Inc. suspicious of others, questions of loyalty of friends/associates, reluctance to confide because they expect to be exploited, reading hidden messages in benign remarks, bearing grudges, easily slighted and quick to retaliate, suspicious of fidelity of partner
○ Does not occur exclusively during schizophrenia or other disorder with psychotic features or medical condition
• Begins by early adulthood
• Unlikely to present for treatment
• 2.3-4% of population
• Aetiology
○ Sparse research
○ More common in relatives of those who have schizophrenia - gentic loading?
○ Low self-esteem
○ Deficits in emotional and social processing

210
Q

Describe schizoid personality disorder

A

• Criteria
○ Pervasive pattern of detachment from social relationships and restricted range of expression of emotions in interpersonal settings
§ Inc. no desire for close relationships, chooses solitary activities, little interest in sexual experiences, takes pleasure in few activities, lacks close friends or confidants, appears indifferent from praise/criticism, shows emotional coldness/detachment/flattened affectivity
○ Does not occur exclusively during schizophrenia or other disorder with psychotic features or medical condition
• Begins by early adulthood
• 2.2-4% of population
• Aetiology
○ Very little research - some call for it to be removed from DSM-V pre-publication
○ Speculation that it is linked to Asperger’s
§ Explains the lack of desire for social interactions
○ Underpowered limbic system
○ Not associated with schizophrenia spectrum disorders
○ High level of dysfunction

211
Q

Describe schizotypal personality disorder

A

• Criteria
○ Pervasive pattern of social and interpersonal deficits marked by acute discomfort and reduced capacity for close relationships as well as by cognitive/perceptual distortions and eccentric behaviour
§ Incl. ideas of reference, odd beliefs/magical thinking, unusual perecptual experiences, odd thinking and speech, suspiciousness/paranoid ideation, inappropriate/constrained affect, odd or eccentric behaviour or appearance, lack of close friends, social anxiety related to paranoia
○ Does not occur exclusively during schizophrenia or other disorder with psychotic features or medical condition
• 1.5-4.6% population
• Aetiology
○ Linked with schizophrenia - could be considered a minor form of schizophrenia
○ Cognitive abnormalities - attention/memory deficits
○ Higher levels of dopamine neurotransmitter
○ Crossover to schizophrenia-spectrum disorders

212
Q

What is antisocial personality disorder?

A

• criteria
○ Pervasive pattern of disregard for, and violation of, the rights of others
§ Incl. failure to conform to social norms/lawful behaviour, deceitfulness, impulsivity or failure to plan ahead, irritability and aggressiveness, reckless disregard for safety, consistent irresponsibility, lack of remorse
○ Individual at least 18 years of age
○ Evidence of conduct disorder before 15 years old
○ Does not occur exclusively during schizophrenia/bipolar
• Prevalence varies depending on sample. Community samples about 3-3.5%
• Over-represented in prison populations
• Aetiology
○ High sensation-seeking, childhood conduct disorder, low psycho-physiological arousal
○ Elevated in family members, as is high levels of criminality, high levels of impulsivity - genetic contribution
○ Low levels of serotonin, frontal problems
○ High levels of childhood aggression and associated with physical abuse, harsh and negative parenting
○ Link with psychopathy
○ What should be the implications for sentencing?

213
Q

What is borderline personality disorder?

A

• Criteria
○ Pervasive pattern of instability of interpersonal relationships, self image affects, marked impulsivity
§ Incl. frantic efforts to avoid abandonment, unstable and intense interpersonal relationships, identity disturbance, impulsivity, recurrent suicidal behaviour/self-harm, affective instability, chronic feelings of emptiness, inappropriate/intense anger, transient paranoid ideation
• Community samples - 1.6-5.9%
• 75% females
• Begins by early adulthood - adolescent diagnosis
• Aetiology
○ Torgersen et al. (2000) found genetic contribution
○ Associated with sexual or physical abuse, and neglectful/invalidating environments
○ Low serotonin
○ Increased hippocampal volumes and heightened activation of the amygdala
○ Have insecure attachment and fearful of abandonment, desire intimacy but anxious about depending on others
• Most individuals with BPD also meet criteria for a mood, anxiety, or substance use disorder
• Some argue it is better defined as a mood/emotional regulation disorder or a form of PTSD
○ Cluster analysis revealed difference between BPD and complex PTSD
○ BPD does not respond to mood stabilising medication as with mood disorders, and treatment for BPD and complex PTSD also differ

214
Q

What is histrionic personality disorder?

A

• Criteria
○ Pervasive pattern of excessive emotionality and attention seeking
§ Incl. uncomfortable when not the centre of attention, interaction characterised by inappropriate sexually seductive or provocative behaviour, rapidly shifting and shallow emotional expression, uses physical appearance to draw attention to self, speech overly impressionistic or lacking in detail, is sugestible, considers relationships more intimate than they are
• Begins by adulthood
• Prevalence: 0.8-1.8%
• More commonly diagnosed in females
• Aetiology
○ Little work
○ Family studies show higher rates of BPD, Antisocial and histrionic PD in relatives
○ Theoretical accounts focus on encouragement of sexualisation, attention-seeking, and role of intense, inconsistent, and non-empathetic parenting interactions
§ Need to be careful not to blame parents - needs to be a combination of several things

215
Q

What is narcissistic personality disorder?

A

• Pervasive pattern of grandiosity, need for admiration, and lack of empathy
○ Inc. grandiose sense of self-importance, preoccupied with fantasies of unlimited success, power, brilliance, beauty, or ideal love, believes that they are special and can only be understood/associated with any other special/high status people or institutions, requires excessive admiration, sense of entitlement, interpersonally exploitative (to achieve own ends), lacks empathy, envious of others, shows arrogant or haughty behaviours or attitudes
• Begins early adulthood
• Not aligned with reality/actual achievements
• Prevalence: 1.2-6.2%
• 50-75% are males
• Aetiology
○ Early childhood experiences: child’s needs for nurturing and affection were not met
○ Kernberg says chronically cold caregivers display either indifference or aggression towards the child. Stone (1993) adds that compensatory beliefs can arise when a child is exposed to parental indifference
○ OR alternative theory - too much praise leading to inflated sense of ego
○ Livelsey et al. (1993) say this PD has the highest genetic loading
• Factor analysis suggests two underlying subtypes (Wink, 1991)
○ Grandiosity or overt narcissism
§ Associated with grandiosity, social charm, failure to respond to needs of others, invulnerability, entitlement, aggression, and dominance
○ Vulnerability/sensitivity or covert narcissism
§ Uses grandiose behaviour to mask hypersensitivity to criticism, self-doubt, deep feelings of inadequacy, incompetence, inferiority, worthlessness, negative affect (high neuroticism)
§ May present as more introverted

216
Q

What is avoidant personality disorder?

A

• Criteria
○ Pervasive pattern of social inhibition, feelings of inadequacy, and hypersensitivity to negative evaluation
§ Incl. avoiding occupational activities with high interpersonal contact due to fear of criticism, unwilling to get involved with people unless certain of being liked, restraint in intimate relationships due to fear of being shamed/ridiculed, preoccupied with social rejection/criticism, inhibited in social settings, views self as inferior/socially inept, reluctant to take personal risks/new activities
• 2.4% prevalence
• Differences in cultural expectations
○ In some cultures it might be normal to stand out, whereas in others it is best to come across as more humble
• Aetiology
○ High in restraint in children, high neuroticism, low extraversion, shyness in childhood, higher incidence of avoidant PD in first-degree relatives
○ Jovev and Jackson (2004) found schemas related to defectiveness and abandonment

217
Q

What is dependent personality disorder?

A

• Criteria
○ Pervasive and excessive need to be taken care of, leads to submissive and clinging behaviour and fears of separation
§ Inc. difficulty making daily decisions w/out reassurance, need for others to make decisions for them, difficulty expressing disagreement due to fear of rejection, difficulty starting things alone, goes to excessive lengths to obtain nurturance and support, feels uncomfortable/helpless when alone, urgently seeks another relationship if one ends, preoccupied with fears of being left to take care of themselves
○ Prevalence is <1%
• Aetiology
○ Separation anxiety disorder and agoraphobia more elevated in family members; high neuroticism, low extraversion
○ Speculation that overprotective attachment - feeling that the world is a dangerous place and that they are incompetent to deal with it alone

218
Q

What is obsessive compulsive personality disorder?

A

• Criteria
○ Pervasive pattern of preoccupation with orderliness, perfectionism, mental and interpersonal control at the expense of flexibility, openness, and efficiency
§ Incl. preoccupied with details, rules, lists etc. until the point of the activity is lost, perfectionism interfering with task completion, excessively devoted to work and productivity to the exclusion of leisure activities/friendships, is overconscientious and inflexible re: morality, ethics, or values, hoarding, reluctance to delegate, money viewed as something to be hoarded for future catastrophes, rigidity, and stubbornness
• Prevalence: 3.2-7.9%
• Diagnosed twice as often in males
• Aetiology
○ High perfectionism
○ Millon and Davis - child learned to suppress their feelings and perform approved behavioural routines in order to avoid punishment or disapproval by parental figures
○ Different from OCD
○ Personality style supported by Western culture

219
Q

Why use semi-structured clinical interviews for personality disorders?

A

• Semi-structured clinical interview which is more reliable than self-report measures
• Encourages the clinician to develop a more thorough and objective approach to assessment
• SCID-5-PD when used with PQ screening questionnaire is less time consuming (mean 36 mins) than comparable measures
○ Screening is used first to identify which category of PD the individual scores the highest in
• PD diagnosis vs PD traits
○ People may present with traits of PD without meeting the criteria of a diagnosis
§ Calls for a dimensional approach
○ Personality lies on a spectrum - DSM-5 disorders on one end of the spectrum

220
Q

What is the aetiology (basic model) of personality disorders?

A

• Aetiology (basic model)
○ Genetic predisposition + life events = personality
○ Personality disorders related to experience of disrupted attachment with primary carers, trauma, neglect, deprivation

221
Q

What are the cognitive models of personality disorders?

A

○ Role of maladaptive core beliefs/schemas (Beck, Young)
§ Eg abandonment, entitlement, unrelenting standards
○ Schema as a filter through which new information is processed
§ Eg perceive ambiguous email as rejection
○ Each PD is characterised by specific maladaptive core beliefs/schema
○ Core beliefs are resistant to change -> maintenance of dysfunctional beliefs, emotions, and behaviours
§ Need something more longstanding than CBT
○ Early maladaptive schema in PDs
§ Highly resistant to change
§ Associated with high levels of affect
§ Significantly impair functioning
§ Individual selectively perceives and distorts information that confirms schema and filters out info that disconfirms them
§ Emotion, body sensations, and behaviours are tied to cognitions
○ Early maladaptive schema result from mixture of biological disposition and repeated failure to meet child’s core emotional needs:
§ Secure attachment to others
§ Develop a sense of identity, competence, and independence
§ To express one’s desires and emotions
§ To have realistic limits set by others so as to learn self-control
§ Spontaneity and play

222
Q

Describe schema perpetuation of personality disorders

A

○ Schema surrender
§ Individual accepts schema as true and fully experiences the associated intense emotions and behaves according to the schema
○ Schema avoidance
§ Blocks thoughts, images, and feelings that are part of the schema due to distressing nature (eg substance use) or avoid situations that trigger schema (eg relationships)
○ Schema overcompensation
§ Reacts in extreme opposite to the schema - underlying schema remains intact but also creates more problems
○ People can be a combination - they can be a schema surrender to one maladaptive schema and an overcompensator for another
§ For treatment, you would identify which maladaptive schemas they have, outline the schemas that were created in childhood, and identify how they respond to the schemas
• Dialectical behaviour therapy (DBT)
○ DBT model and therapy (Linehan) based on the following
§ Dysfunctional emotion regulation is fundamental - part biological/part experiential
§ Temperament - high in neuroticism, heightened baseline arousal, increased intensity of responses to emotional stimuli
§ Child is subjected to drastically invalidating environments eg deprivation, neglect, and physical and emotional abuse

223
Q

What are some issues with the DSM conceptualisations of personality disorders?

A

ome DSM PD criteria are behaviours, eg criminal acts, others are traits eg feeling empty
○ Some PD criteria are harder to assess eg identity disturbance, than others eg impulsivity
○ Diagnostic criteria determined by consensus
§ Can be hard to fnd that consensus
○ Some features of PDs are found in other disorders and also in people without PDs

224
Q

How helpful are categories?

A

○ Pros
§ Guide treatment
§ Helps with diagnosis
§ Help provide clients with improved understandings of their struggles
§ Ease communication (clinical and research)
○ Cons
§ Not much evidence for effective treatment
§ Can increase stigma, and viewed as stable and pervasive
§ Are we better off addressing on symptom levels eg specific pattern of the behaviour)

225
Q

Explain the push for dimensional categorisation

A

○ Hopwood et al. argued
§ There is no/poor empirical evidence supporting the hypothesis that personality disorders are categorical
§ Low reliability of categories
§ Substantial comorbidity
§ Individual can meet criteria for category in numerous ways
§ Littler treatment progress
□ Treatment BPD non-specific
○ Current system contributes little, requires change to be empirically supported

226
Q

What is the Big Five Theory - dimensional theory (NEO)

A

○ Five-factor model
○ Opennes
○ Conscientiousness
○ Extraversion
○ Agreeableness
○ Neuroticism
○ The use in clinical practice
§ Diagnosis
□ Can provide an objective measure of personality traits related to PD diagnoses
§ Feedback
□ Of results may encourage engagement of client in treatment, aid development of insight
§ Useful in assessing personality resources
§ Can assist selection of optimal treatment/suitability for therapy
□ Low C and A linked to poor therapy outcome
□ Low O scorers respond better to supportive ‘common sense’ approach to biofeedback
□ High O scorers make better use of imagery techniques
□ Depressed high E scorers respond better to interpersonal therapy (IPT) than to antidepressants - opposite pattern for depressed introverts
§ Assessment of the person
□ Can assist in understanding of basic emotional, interpersonal, attitudinal and motivational styles

227
Q

What is TCI - an alternative perspective to the Big Five theory?

A
○ Robert Cloninger - Temperament and Character Inventory (TCI)
		○ Seven dimensions
			§ Temperament
				□ Novelty seeking (dopamine)
				□ Harm avoidance (serotonin
				□ Reward dependence (norepinephrine/GABA)
				□ Persistence
			§ Character
				□ Self-directedness
				□ Cooperativeness
				□ Self-transcendence
			§ Found that people with bulimia score high on novelty seeking, and low on self-directedness and cooperativeness
228
Q

What is the ICD-11 proposed model for personality disorders?

A

○ Focus on impairment of self and interpersonal functioning , global assessment
§ Classified according to severity (mild, moderate, severe)
§ One or more prominent trait qualifiers
□ Negative affectivity
□ Detachment
□ Dissociality
□ Disinhibition
□ Anankastia
® High perfectionism and rigid personality trait
§ Much more dimensional than DSM
§ Includes borderline patterns qualifier
§ More of a hybrid than the other options because of the trait aspects

229
Q

What are the treatment approaches towards personality disorders?

A

• Psychosocial
○ CBT or variants
§ Eg Young Schema therapy
§ Dialectical behaviour therapy - really effective with BPD
§ CAT
○ Group and individual
• Pharmacological
○ Behaviour traits associated with personality disorders associated with neurochemical abnormalities
○ Nearly all clinical trials have been with BPD (70% from 2008 research review)
• Outcomes
○ Cluster A: adaptive failures and least treatable
○ Cluster B: major social problems - variable treatment success
○ Cluster C: Least severe adaptive failures, best outlook
• Issues
○ Comorbidity with other disorders
§ Which came first? Timeline can be helpful
○ No consensus on how to measure improvement
○ Social and interpersonal function often remain impaired
○ Major lack of evidence-based treatments
• Stigma
○ Stigam associated with PDs
○ PDs often seen as egosyntonic - part of who the person is?
○ Understanding and empathy vital
§ Person is doing their best to get through life as best as they know how
○ Aetiology - emphasis on parental behaviour
§ Careful of blame - most parents are trying their best given their personal resources
• Strengths-based approach
○ Current emphasis in mental health is on categorising individuals according to pathology
§ Focused on pathology
§ Low self-esteem, stigma, quality of life
§ Considered chronic
○ Instead, focusing on individual’s attributes that promote health
§ Mental health is seen as normal part of human life
§ Focus on living meaningful life despite mental illness
§ Greater autonomy in recovery
○ Strengths-based approach associated with better academic, social, and behavioural outcomes, and increased life satisfaction, but more research needed

230
Q

What is the criteria for obsessive compulsive disorder?

A

• Criteria
○ Obsessions and compulsions are recurrent and persistent
○ Individual recognises they are excessive and unreasonable
○ Obsessions/compulsions cause marked distress, re time consuming (>1 hr a day), and significantly interfere with functioning and relationships

231
Q

What are obsessions?

A

• Obsessions
○ Persistent ideas, thoughts, impulses, or images that are experienced as intrusive and inappropriate and cause marked distress or anxiety
○ Individual recognises thoughts are a product of their own mind
§ Ie not delusions
○ Common types
§ Fears of contamination
§ Repeated doubts (safety, scruples)
§ Need to have things in a particular order
§ Sexual, horrific, or blasphemous imagery
§ Aggressive or inappropriate impulses
§ Nonsensical thoughts or images

232
Q

What are compulsions?

A

○ Repetitive behaviours (eg handwashing, checking) or more mental acts (praying, counting), the goal of which is to prevent or reduce anxiety
§ Anixety may go down temporarily but the thought/obsession will not go away - will be repeated
○ Can include rigid/stereotyped acts according to elaborate rules without any real explanation of them
○ Common types
§ Washing and cleaning
§ Checking
§ Repeating
§ Ordering
§ Mental rituals
§ Reassurance seeking
§ Compulsive shopping

233
Q

What are the rates of OCD symptoms in the general population?

A

○ Up to 80% of population may experience intrusive, unpleasant, and unwanted thoughts
○ More than 50% of the population may engage in ritualised behaviour
§ Crino, Slade, and Andrews, 2005
○ Concerns about harm/checking are most commonly experienced, followed by somatic obsessions, and symmetry and ordering in general population

234
Q

What are the rates of OCD according to diagnostic criteria?

A

○ 12 month prevalence: 1.2%
○ Lifetime prevalence: 2.3%
○ No difference in prevalence rates between male and female adults
○ Average age of onset ~ 19 yrs, but childhood onset and later age onset not uncommon
○ No difference between OCD and non-OCD in gender, marital status, education, migration status, urbanicity
○ Fluctuating coarse of illness in conjunction with stress levels
○ Chronic course in approx. 50% of cases

235
Q

What are the onset, gender, and common symptom profiles of OCD?

A

• Childhood onset OCD
○ Between one third and one half of adult patients report that they first developed OCD during childhood
○ Childhood OCD more common in boys than girls? Not sure why
• Common symptom profiles
○ 90% of patients with OCD have obsessions and compulsions
○ 8-20% have obsessions and mental rituals, but not behavioural compulsions
• OCD & gender
○ Equally distributed amongst male and female adults
○ But there are differences in the presentation of OCD
○ Females are more likely to experience obsessions related to harm and checking, females are more likely to experience symptoms across the board
○ Men’s experiences of sexual or religious symptoms are more common and more severe,

236
Q

Explain the comorbidities and causes of OCD

A
• Comorbidity
		○ The norm
		○ Major depressive disorder: 28.4%
		○ Obsession Compulsive PD: 24.5%
		○ Generalised anxiety disorder: 19.3%
		○ Specific phobia: 19.2%
		○ Social phobia: 18.5%
		○  Also substance use 
	• Causes of OCD
		○ Learned responses
		○ Genetic predisposition
			§ Mutations in hSERT gene linked to OCD
		○ Environmental factors 
			§ Early life experiences may increase vulnerability
		○ Brain structure and function
237
Q

What is the cognitive model of OCD

A

○ Begins with premise that intrusive thoughts are normal
○ However, certain individuals place meaning on these thoughts and thus respons to them in some way
○ These responses increase vigilance for the intrusive thoughts and protects the meaning of the intrusion
§ Salkovskis, 1985

238
Q

What are the cognitive factors of OCD?

A

○ Intrusive thoughts may become obsessions if they are evaluated as :
§ Overly important
§ Highly threatening
§ Requiring complete control
§ Necessitating a high degree of certainty
§ Associated with a state of perfection
□ Clark and O’Connor, 2005

239
Q

What are the criteria for body dysmorphic disorder?

A

○ Preoccupation with one or more perceived defects or flaws in physical appearance that are either not observable or appear slight to other people
○ At some point during the course of the disorder, the individual have performed repetitive behaviours (eg mirror checking, skin picking) or mental acts (comparing his or her appearance with other’s) in response to the appearance concerns
○ The preoccupation causes clinically significant distress or impairment in social, occupational, or other important areas of functioning
○ Used to be known as dysmorphobia
○ Specify if:
§ Muscle dysmorphia: preoccupation with the idea that his or her body build is too small or insufficiently muscular
□ Impacts males more than females
• Lots of cross over with eating disorders - can be hard to distinguish, requires good level of history-taking
○ Often the differentiating factor between BDD and anorexia nervosa is the desire for thinness, and the enagement in binge-eating/purging with bulimia

240
Q

What are the prevalence, onset, and course of body dysmorphic disorder?

A

• Prevalence
○ 0.7-2.4% adult population
○ Generally recognised as underdiagnosed
○ Higher rates among dermatology, cosmetic surgery, adult orthodontist and oral/maxillofacial surgery patients
• Onset and course
○ Mean age of disorder onset is 16-17, although not usually diagnosed until 10-15 years later
○ Patients generally present to services for secondary or associated disorders (eg OCD, depression etc)
○ Approximately 25% of patients attempt suicide
○ Disorder is usually chronic, although improvement is likely when evidence-based treatment is received
○ Individuals with disorder onset before age 18 are more likely to attempt suicide, have more comorbidity, and have gradual (rather than acute) disorder onset than those with adult-onset body dysmorphic disorder

241
Q

Explain the gender differences of body dysmorphic disorder

A

○ No difference in prevalence rates
○ More similarities than differences in more clinical features - for example, disliked body areas, types of repetitive behaviours, symptom severity, suicidality, comorbidity, illness course, and receipt of cosmetic procedures
○ However, males are more likely to have genital preoccupations, and females are more likely to have a comorbid eating disorder
○ Muscle dysmorphia occurs almost exclusively in males

242
Q

What is the impact of body dysmorphic disorder on functioning and the cognitive processes?

A

• Impact on functioning
○ Can range from moderate (eg avoidance of some social situations) to extreme and incapacitating (eg hospitalisation/being completely housebound)
• Cognitive processes
○ Compare to healthy individuals, people with BDD:
§ Evaluate appearance more negatively
§ Endorse assumptions about appearance such as “if my appearance is bad, then I am worthless)
§ Overvalue physical appearance and attractiveness
§ Experience more anxiety and discomfort after mirror gazing
§ Experience more distress and self-focussed attention after mirror gazing
§ Enage in ruminative thinking
§ Engage in repeated reviews of past-appearance related experiences
§ Kollei & Martin, 2014

243
Q

Describe the relationship between body dysmorphic disorder and medical interventions

A

• BDD and medical interventions
○ Of 268 patients seeing a dermatologist ~ 12% met criteria of BDD
○ Approx. 45% of BDD patients seeking dermatological treatment and 23% seeking plastic surgery
○ Therefore, people with BDD
§ Make up a significant proportion of people seeking assitance from dermatology or plastic surgery
§ BUT, they are also unlikely to be happy with the result, may return time and time again for treatment and can be litigious
• BDD and culture
○ Link between BDD and social beauty expectations/standards

244
Q

What are the criteria for hoarding disorder?

A

○ Persistent difficulty discarding or parting with possessions regardless of their actual value
○ The difficulty is due to a perceived need to save the items and to distress associared with discarding them
○ The difficulty discarding possessions results in the accumulation of possessions that congest and clutter active living areas and comprimises their intended use. If living areas are uncluttered, it is only because of the interventions of third parties
○ The hoarding causes marked distress or impairment in social, occupational, or other important areas of functioning

245
Q

What is the prevalence of hoarding disorder?

A

○ Estimated to be between 2-6% adults in Europe and US
○ Nordsletten et al. - 1.5% adults in South london
○ Affects males and females - possibly more common in males (although more females present for treatment)
○ More common in older than younger adults
○ Thought to be underdiagnosed

246
Q

What are the cognitive features associated with hoarding disorder?

A

○ Control over possessions
○ Concerns about memory
§ But still unable to find things
○ Responsibility over possessions

247
Q

Describe the impacts of animal hoarding

A

○ The compulsion to collect an own animals for the sake of caring for them that results in accidental or unintentional neglect o rabuse
○ Animals may provide a conflict-free relationship with the individual, unconditional love
○ Alternatively, perceptions of being a refuge for unloved animals may provide the individual with a sense of purpose
○ BUT in many cases, everyone suffers with animal hoarding - the animals, the hoarder, and those who love the animal hoarder

248
Q

What are the criteria for trichotillomania (hair pulling)?

A

○ Recurrent pulling out of one’s hair, resulting in hair loss
○ Repeated attempts to decrease or stop hair pulling
○ The hair pulling causes clinically significant distress or impairment
○ The hair pulling or hair loss is not attributable to another medical condition
○ The hair pulling is not better explained by the symptoms of another mental disorder

249
Q

What is the prevalence and course of trichotillomania (hair pulling)?

A
• Prevalence
		○ 1-2% adults
		○ Perhaps more females
	• Course of illness
		○ Usually chronic
		○ Can wax and wane
250
Q

What are the functional impairments of trichotillomania (hair pulling)?

A

○ Social/occupational
○ Musculoskeletal injury (eg carpal tunnel, back, shoulder, neck pain)
○ Blepharitis
○ Dental damage
○ Swallowing or hair may lead to hairballs

251
Q

What are the criteria for excoriation (skin picking)?

A

○ Recurrent skin picking resulting in lesions
○ Repeated attempts to stop skin picking
○ Causes clinically significant disress or impairment
○ Not attributable to physiological effects of substance use or another medical condition
○ Not better explained by medical condition

252
Q

What What is the prevalence and course of excoriation (skin picking)?

A
• Prevalence
		○ 1-2% adults
		○ Maybe more females
	• Course of illness
			○ Usually chronic
			○ Can wax and wane
253
Q

What are the functional impairments of excoriation (skin picking)?

A

• Functional consequences
○ Social/occupational
○ Tissue damage, scarring, infection
○ Frequently requires antibiotic treament

254
Q

What are the Psychological aspects of trichotillomania and excoriation?

A

• Motivated by stimulation of positive mood or feelings or regulation of states of high or low arousal
• Approximately 1/5 or 1/3 of people with SPD or trich report being in a trance/feeling mesmerised
• Substantial proportion of sufferers in both groups report little or no reflective awareness in the act as it occurs
○ Two subtypes
○ Automatic pulling/picking: occurs out of reflective awareness
○ Focuses pulling/picking: happens in full awareness in response to urges or negatie affective states
• Psychological consequences
○ Shame, distress, embarrassment
○ BUT
○ Hair pulling and scratching can also reduce unpleasant emotions

255
Q

What are neurodevelopmental disorders?

A

• A group of disorders with onset in childhood (typically before puberty), though not always diagnosed in early developmental period
• High heritability
• More common in boys than in girls
• Typically multifactorial in origin (singular causes are rare)
• A range of developmental deficits impacting on functioning across domains
• Types:
○ Intellectual Disability (Intellectual Developmental Disorder) & Global Developmental Delay
○ Communication disorders
§ Language disorder,
§ Speech Sound Disorder
§ Social (Pragmatic) Communication Disorder
§ Childhood Onset Fluency Disorder (stuttering)
○ Specific Learning Disorders
§ Reading, writing, mathematics
○ Autism Spectrum Disorder
○ Attention Deficit Hyperactivity Disorder
○ Motor Disorders
§ Developmental Coordination Disorder
§ Stereotypic Movement Disorder
§ Tic Disorders

256
Q

What are the core features and prevalence of intellectual disabilities?

A
• Core features 
		○ Deficits in intellectual functioning
			§ Eg reasoning, problem solving, planning, abstract thinking, judgement, academic learning , and learning from experience
		○ And deficits in adaptive functioning
			§ Eg developmental and sociocultural expectations for personal independence and social responsibility
	• Prevalence
		○ 1-3% of population
		○ More common among males - 1.5:1
257
Q

What are the risk factors of intellectual disabilities?

A

○ Overview
§ At least 500 causes known
§ Many cases are of unknown aetiology
○ Prenatal and birth complications
§ Prenatal exposures - eg alcohol, lead etc
§ Prenatal iodine deficiency
§ Maternal infections (eg rubella)
§ Complications of birth/prematurity (eg hypoxia, periventricular haemorrhage)
○ Environmental factors
§ Severe malnourishment
§ Brain radiation
§ Acquired brain injury - eg infections, TBI, stroke
○ Medical conditions
§ Neurological disorders (eg epilepsy)
§ Metabolic conditions (eg phenylketonuria)
○ Chromosomal abnormalities/genetic conditions
§ Down syndrome, Fragile X Syndrome, Prader-Willi Syndrome

258
Q

Describe Autism Spectrum disorder

A

• Core features
○ Persistent deficits in social communication and social interaction across contexts, and restricted, repetitive patterns of behaviour, interests, or activities
• Prevalence
○ 1 in 54
○ Males:females (4:1) but there is under-identification in girls/women
• Risk factors
○ Overview
§ Aetiology poorly understood (despite extensive research)
§ Many pre-natal biological/environmental factors under investigation but few clear findings
○ Known risk factors include
§ Strong familial influence
§ Differences in early brain development
□ Early brain overgrowth - marked in frontal areas, reduced cortical pruning, atypical patterns of activation/connectivity - various regions & networks
□ Advanced parental (esp. paternal age)

259
Q

What are the core features of ADHD?

A
• Core features
		○ A persistent pattern of inattention and/or hyperactivity-impulsivity across settings that interferes with functioning or development 
		○ Subtypes
			§ Predominantly inattentive
			§ Predominantly hyperactive
			§  Combined (75% of children)
	• Prevalence
		○ 5-7%
		○ Boys > Girls (3:1) - differences only for combined and hyperactive subtypes
260
Q

What are the risk factors of ADHD?

A

○ Genetics
§ Strong heritability (>70%)
§ Multiple genes; particularly those involved in dopamine and serotonin pathways
§ High prevalence associated with some genetic conditions - eg Fragile X
○ Neurobiological findings
§ Differences in regions involved in attention and executive and inhibitory control
§ Structural differences: esp. in prefrontal areas
§ Neurochemical differences: lower Dopamine and Norepinephrine (Noradrenaline) levels (reuptake problems)
○ Environmental factors include
§ Maternal smoking & drinking during pregnancy
§ Low birth weight & prematurity
§ Toxins - eg lead and other pollutants
§ Higher prevalence in context of psychosocial adversity

261
Q

What are the DSM 5 Disruptive, impulse-control, and conduct disorders?

A
• Conditions involving problems in the self-control of emotions and behaviours. While other disorders in DSM-5 may also involve problems in emotional and/or behvaioural regulation, the disorders in this chapter are unique in that these problems are manifested in behvaiours that violate the rights of others (eg aggression, destruction of property), and/or that bring the individual into significant conflict with societal norms or authority figures
	• Types
		○ Oppositional Defiant Disorder
		○ Conduct Disorder
		○ Intermittent Explosive Disorder
		○ Pyromania
		○ Kleptomania
		○ Antisocial Personality Disorder
		○ Other Specified and Unspecifie
		○ d Disruptive, Impulse Control, and Conduct Disorders
262
Q

How common are mental health conditions in childhood?

A

○ Females: 11.5%
○ Males: 16.3%
○ People in general: 13.9%
§ Only 56% had used services for emotional and behavioural problems in the last 12 months
• Lifetime (childhood) prevalence
○ Around 20% of individuals experience a psychological disorder at some time during childhood

263
Q

What are common types of mental disorders seen in children?

A

○ ADHD: 7.4%
○ Anxiety disorders: 6.9%
○ Major depressive disorder: 2.8%
○ Conduct disorder: 2.1%

264
Q

What is the comorbidity of mental disorders in children?

A

○ Around 40% of children with on mental disorder also have another
§ Adolescents with depression
□ 50-75% also have an anxiety disorder
§ Children with an Anxiety Disorder
□ 40-60% have at least one other anxiety disorder
§ Children with Autism Spectrum Disorder
□ Up to 80% have clinically significant anxiety symptoms ; 40-60% have an anxiety disorder
§ Adolescents with Oppositional Defiant Disorder
□ Around 90% meet criteria for another disorder
® Anxiety disorders, depression, substance use disorders, ADHD
○ High comorbidity could reflect
§ Shared aetiology?
§ Challenges with drawing categorical boundaries?
§ Impairments associated with one disorder become risk factors for another?

265
Q

What is the prevalence of childhood mental disorders?

A

• Prevalence by age
○ Overall prevalence: adolescents > younger children
○ But also disorder-specific findings
§ Depression, anxiety disorders, eating disorders:
□ Higher prevalence in adolescents than younger children
§ ADHD, ODD
□ Higher prevalence in younger children than adolescents
• Prevalence by sex
○ Depression, Anxiety disorders, PTSD, Eating disorders
§ More prevalent in girls
○ ODD and ADHD, ASD, Specific Learning Disorders
§ Occur more frequently in boys

266
Q

Describe the interaction between age and sex for childhood mental disorders

A
○ Depression
			§ Equal prevalence in pre-adolescents
			§ Girls > boys in adolescence
		○ ODD
			§ Boys > Girls in pre-adolescents
			§ Equal prevalence in adolescence
267
Q

What are disorders with increasing childhood prevalence?

A

○ Depression
§ 9% for those born in 1990s -> 15% for millennials
○ Anxiety disorders across childhood
§ 51% reported increase between 2004 and 2017
○ Autism Spectrum Disorder
§ From 1 per 5 000 in 1990 -> 1 in 88 in 2012 -> 1 in 54 in 2016
○ Increasing rates could reflect
§ Increased awareness/understanding?
§ Decreased stigma?
§ Changed diagnostic criteria?
§ Risk factors more prevalent?
• Childhood mental health disorders have associated
○ Distress
○ Functional impairment
○ Cascading effects on development

268
Q

Explain the fact that many adult disorders have childhood origins

A
• Kessler et al (2005): half of adults with mental health disorders: onset of the disorder by 14 years of age, and 75% before 24 years old
	• Barriers to accessing services
		○ Stigma? (Parents, children)
		○ Availability/accessibility?
		○ Under-identification?
269
Q

What are categorical descriptions of childhood abnormality?

A

○ provide a shared language to aid understanding
○ Guide intervention
○ Facilitate access to funding and services
○ Provide validation/legitimacy; help to avoid conceptualisations of ‘blame’

270
Q

What are the challenges with categorical descriptions of childhood abnormality?

A

○ Sub-clinical presentations less readily described/gain less attention
○ Locates problem within the child
○ Children are a ‘work in progress’
○ Role of labels in shaping subsequent development
○ Instability of diagnosis

271
Q

Describe developmental continuities and discontinuities in terms of childhood abnormality?

A

○ We may see
§ Developmentally transient problems
§ Homotypic continuity (continuation of the same disorder/same symptom profile from childhood through to adulthood)
§ Heterotypic continuity (the manifestation of psychopathology changes across development
• Developmental factors can impact on clarity re diagnosis
○ Younger children can struggle to reflect on/describe internal experiences
○ Looking for behavioural indicators; relying on others’ reports
○ Parent-child concordance poor (esp. for internalising)
○ Establishing distress and impairment - subjectivity: who do we ask?
○ High levels of comorbidity
○ Wide range for what is typical for any given age
○ Heterogeneity of presentations within and across developmental stages

272
Q

What is developmental psychopathology?

A

○ A broad integrative, cross-disorder approach to studying the developmental processes and pathways that lead to adaptive and maladaptive behaviour across the lifespan
○ Involves understanding the interplay between
§ Changing systems within and outside of the person across multiple levels of functioning, from epigenetic and neurobiological, to cultural and societal
□ Multi-level perspective
○ Key concepts
§ Children are shaped by, and shape, their environments
□ Children are embedded within systemic contexts
® Bronfenbrenner’s Social Ecological Model
□ With reciprocal influences
® Overprotective/involved parenting leads to behavioural inhibition/anxiety, which leads to further over-protective/involved parenting
□ Cascading effects on development

273
Q

Describe normative development

A

□ At each stage of development, there are stage-salient issues (Developmental tasks) to be confronted and mastered (across domains)
□ Whether these are resolved in adaptive or maladaptive ways influences future adaptation
□ Psychopathology as adaptational failure
□ Prenatal period –> infancy:
® Physical growth
® Brain development
® Establishing an attachment to one of more specific caregivers
® Differentiation of self from the environment
® Acquiring functional language
® Learning to walk
□ Preschool –> middle childhood
® Separation form caregivers
® Regulating emotions and behaviours
® Acquiring academic skills
® Developing peer relationships
® Rule-governed behaviour
□ Adolescence
® Establishing autonomy from parents
® Consolidating close peer relationships
® Preparing for a job/career/further education
® Exploring/developing various aspects of identity

274
Q

Describe the developmental pathways

A

Multiple factors (individual and systemic) interact dynamically and bi-directionally to influence the course of an individual’s development
There are individual risk-factors, vulnerabilities, and protective factors for each child
Genetic, biological, and systemic factors interact to influence (but not to determine) outcomes: Probabilistic epigenesis
Various pathways may stem from similar beginnings
□ Differing beginnings can lead to similar outcomes
□ Vulnerability
® A biologically-based factor or trait that renders individuals more susceptible to developing psychopathology in the face of risk factors
® Eg genetic predisposition

275
Q

What are risk factors associated with developmental psychopathology?

A
□ Risk-factors
					® Environmental experiences or circumstances that increase the likelihood that someone will have difficulty with adaptation eg:
						◊ Poverty
						◊ Parental psychopathology
						◊ Community violence
						◊ Family violence
						◊ Child maltreatment
					® Three types of adverse childhood experiences (ACEs)
						◊ Abuse
							} Physical 
							} Emotional
							} Sexual
						◊ Neglect
							} Physical
							} Emotional
						◊ Household dysfunction
							} Mental illness
							} Incarcerated relative
							} Mother treated violently
							} Substance abuse
							} Divorce
						◊ 64% of children have at least 1 ACE, with physical abuse being the most common (28.3%)
276
Q

What are protective factors associated with developmental psychopathology?

A

® Factors that promote or maintain healthy development in the face of risk
® Internal resources or external/environmental resources eg:
◊ Good intellectual functioning
◊ An easy temperament
◊ High self-efficacy
◊ An authoritative parenting style
◊ A positive, stable relationship with a caregiving figure
◊ Positive connections with adults outside of the family
◊ A talent/hobby valued by adults/peers

277
Q

What is the significance of resilience for developmental disorders?

A

• Resilience
○ Successful adaptation despite exposure to considerable risk
○ Not a static trait
○ Can vary across contexts and time
○ In the face of risk factors and vulnerabilities, some will show resilience

278
Q

What is addiction?

A

• Refers to the disease process underlying a substance use disorder or similar
• The term itself is not a diagnosis or medical label
• History
○ In the Middle Ages, alcolol was preferred to water because of the lack of clean water
§ The Christian church emphasised an idea of ‘moderation’
§ Use beyond ‘moderation’ was viewed as a character flaw for succumbing to temptation (an issue of the spirit)
○ Wasn’t until mid 1800s that scientists began to explore the idea that substance use may be a medical condition
○ Current separation of drug/alcohol treatment from other mental health treatment is partially a function of historic separation (drug/alcohol thought to be indicative of weak character)
§ Idea that we have to get the person ‘clean’ before we can treat them
§ This could be harmful if substances are used as a coping mechanism - taking it fully away could complicate the mental health issue

279
Q

What is the preferred terminology of addiction?

A

○ When taking about substance:
§ Use
□ Ay use of a given substance/drug
§ Misuse
□ Harmful use of substances (incl. use for non-medicinal purposes)
§ Abuse (DSM-IV category)
□ A pattern of repeated drug or alcohol use that often interferes with health, work, or social relationships
□ Considered less serious than dependence
§ Dependence (DSM-IV category)
□ An adaptive state that develops from repeated drug administration, and which results in (physical or psychological) withdrawal upon cessation of drug use
§ Use Disorder (DSM 5 category)
□ Takes the place of Abuse/Dependence as of DSM-V

280
Q

What classifies mild/moderate/severe substance use disorders?

A

§ Mild substance use disorder: 2 or 3 are met
§ Moderate: 4 or 5 of criteria are met
§ Severe: 6+ criteria are met
○ Other options for assessing severity
§ Extent of functional impairment
§ Amount regularly consumed
□ Binge drinking episode (4 drinks for women, 5 for men)
□ At least weekly marijuana use
§ Problems
□ Small amounts of use can lead to high levels of impairment
□ Amounts are hard to estimate across drugs

281
Q

What are the changes from DSM-IV to DSM-V for substance use disorders?

A

○ DSM-IV allowed people who were charged for merely carrying a joint in their pocket as having a substance abuse disorder
○ Some issues with abuse and dependence
§ Abuse was defined to be a single issue, which contradicts the idea of a syndrome (which is a collection of symptoms)
§ Moreover, the legal problems criterion created sociocultural bias (many substances carry legal penalties)
○ Certain abuse symptoms may suggest more functional impairment than certain dependence criteria (even then, former is meant to be precursor to the latter)
○ Abuse does not always precede the dependence and cases of dependence do not always meet criteria of abuse

282
Q

What is craving?

A

• Craving = a strong desire or urge to use the substance, or such a strong desire to use that it interferes with thoughts
• Added into DSM-5
• How it works
○ Distal factor affecting intention to use –> Either craving or coping mechanism –> Behavioural outcome (using or refraining from the drug)
○ Eg: hard day at uni –> walk past The Clyde (cue) –> start craving a beer –> decide to go into or not into the pub and drink
○ While it is a choice, it is not necessarily a conscious choice - many other things affect it

283
Q

What is the data on drug use?

A

• Most commonly used drug is alcohol which by far outweighs all others
○ By 2017, 60% of individuals had used tobacco, and a close third and fourth were cannabis and energy drinks
○ Tobacco use has declined over recent years, but caffenated energy drinks are not often talked about being addicitive
• Most common drug use
○ Marijuana, then pain medication

284
Q

Describe the epidemiology of substance use disorders?

A
• Alcohol use disorder
		○ Most common
		○ Use: 8.5%
		○ Abuse: 4.65%
		○ Dependence: 3.81
	• Any illicit drugs
		○ Use: 2%
		○ Abuse: 1.37
		○ Dependence: 0.63%
285
Q

What is the gateway hypothesis of substance use disorders?

A
  • Popularised by Kandel
    • Theory is that marijuana is a gateway drug and leads to use of more illicit drugs
    • Complicated, because most people start with alcohol/cigarettes, switch to the other one of those two
    • But theory is that marijuana is gateway to using more illicit drugs
    • Could be just because it has higher availability of the drug is easier, so it makes sense to start with that
286
Q

Explain why the substance itself doesn’t matter for substance use disorders

A

What causes people to develop a SUD, the issue isn’t what drug they use, but when they use it
Highest predictor of whether someone will develop an SUD, is age of first use
People whose first substance use was prior to age 15 were much more likely to develop an SUD
• Most people start using drugs in early adulthood (between 18-20)

287
Q

What are the dependence rates for common drugs?

A
• Dependence among users
		○ Tobacco has 30% dependency rate (most)
		○ Heroin is approx. 23%
		○ Cocaine is approx. 16%
		○ Alcohol is approx. 15%
288
Q

What are the three types of dependence?

A

Psychological
Physiological
Combination
Most substances’ likelihood to become dependent on a substance peaks early and then flattens out, but for tobacco it continually rises
§ Continuing to use most drugs over time doesn’t necessarily make people more likely to become dependent except for tobacco

289
Q

What is abuse potential?

A

○ Partially relates to how quickly a drug has its effects (varies by drug and route of administration)
○ The quicker the drug acts, the faster is usually stopsacting
§ Abuse potential is higher to try and curb the down swing
○ Half-life (how long it takes your body to clear the drug) is also important to abuse potential
§ Short half lives also lead to high abuse potential
○ Quick up + quick down = high abuse potential

290
Q

Describe caffeine withdrawal

A
○ Withdrawal effects of caffeine can reliably be demonstrated in nearly 100% of individuals with as little as 100mg of caffeine (1 cup of coffee) per day
		○ Withdrawal entails
			§ Headache
			§ Fatigue 
			§ Anxiety
			§ Concentration difficulties
			§ Depression/flat affect
			§ Irritability
			§ Tremors
			§ Low energy
291
Q

Describe alcohol withdrawal

A
○ Symptoms
			§ Tremors
			§ Insomnia
			§ Nausea/vomiting
			§ *Transient hallucinations
			§ Psychomotor agitation
			§ Anxiety
			§ *seizures
			§ Delirium tremens (5-20% of patients experience when undergoing detox): hyperadrenic state, disorientation, tremors, diaphoresis, impaired attention and consciousness, and visual and auditory hallucinations
		○ Alcohol should never be quit cold turkey, should be monitored in a hospitalisation setting when easing off, and often medications are needed for seizures
292
Q

Describe cannabis withdrawal

A
○ Reported in ~1/3 of users in general population
		○ Reported by ~50-95% of heavy users
		○ Symptoms
			§ Most common
				□ Anger, aggression, irritability
				□ Anxiety/nervousness
				□ Decreased appetite/weight loss
				□ Restlesness
				□ Sleep difficulties including strange dreams
			§ Less common symptoms
				□ Chills
				□ Depressed mood 
				□ Stomach pain/physical discomfort
				□ Shaking
				□ Sweating
			§ Not life-threatening
293
Q

What does substance use disorder treatment usually entail?

A

○ Psychotherapy and/or brehavioural counselling
○ Medication
○ Management of withdrawal symptoms
○ Evaluation/treatment of co-occurring mental health conditions
○ Relapse prevention
○ Detoxification (being admitted in an in-patient setting, eg for alcohol)

294
Q

What are the treatment considerations of substance use disorders?

A

○ Detoxification requires medical oversight to manage acute physical withdrawal symptoms. It is not necessary for all drugs
○ Some drugs are harder to treat then others
§ Alcohol/benzodiazepine treatment can be life-threatening (high likelihood of physical withdrawal/seizures) - requires medical monitoring
§ Treatment of opioid use disorders is tricky because detoxification can lead to increased likelihood of over dose upon discharge
□ Because tolerance is lowered
○ NIDA has proposed treatment principles (evidence-based)
§ None of these have very high effect sizes, which means we need to combine different elements of treatment for biggest effect
§ Matching treatment to the needs/desires of the client (d=0.24)
§ Deal with mutiple mental health/medical needs of the client (d=.32)
§ Remaining in treatment (complete, d=0.28)
§ Receive counselling
□ Contingency management (d=0.21) more effective than CBT (d=0.11)
□ Therapeutic community is helpful (d=0.36)
§ Receive drug testing (d=0.18)
§ Meta-analysis with adolescents suggests that family therapy may be the most effective

295
Q

What are typical treatment approaches for substance use disorders?

A

○ Alcholics/Narcotics anonymous
§ Group based treatment based onprinciples of 12 steps (abstinence)
§ In abstinence-based programs, an lapse is seen as a relapse and the person has to restart from square one (issue with alcoholics/narcotics anonymous)
§ Can encourage individual to go on a bender, because one sip is essentially equivalent to a whole slab
○ Behavioural therapy
§ Contingency management (uses principles of reinforcement, rewards, punishment)
○ CBT
§ Recognition of triggers/cues for use and facilitation of coping strategies
○ Harm/reduction minimisation
§ Goal of reducing harmful use to less harmful use or reducing means of use to less harmful approach. Focus on functionality
○ Motivational enhancement therapy
§ Quite effective
§ Effort to facilitate movement through stages of change

296
Q

Explain the use of harm/minimisation approaches to substance use disorders in comparison to abstinence

A

○ Abstinence may not be for everyone, so the goal is not necessarily abstinence, but just a reduction from high risk to low risk

297
Q

Describe the stages of change approach to substance use disorders

A

○ People that are engaged with current substance use/dependence are not really thinking about change
○ Idea is to move them through the stages towards change
○ Start with raising why the individual may want to change, while recognising that there is a loss in quitting

298
Q

What is the aetiology of substance use disorders?

A

• Impaired control vs choice
○ People re unable to do things for themselves vs it being a conscious, decisional choice
○ Disease model of addiction suggests use behaviour is functionally underpinned by a loss of control (ie individual cannot help but use substance)
§ Alternative approach is that it is a rational choice
○ In between the two is an argument that it is an impairment in decision-making processes
• Biological factors
○ Deficits in neural circuitry underpinning incentive salience, executive function, and abnormal reward/stress response fuel addiction cycle of binge/intoxication, withdrawal, and preoccupation

299
Q

Describe the prohibition/legalisation controversy surrounding illicit drugs

A

§ Alcohol
§ In US in early 1900s, government prohibited alcohol
§ During this period, alcohol use did not stop, rather black market trading began
§ This led to the product becoming less regulated, resulting in a spike in alcohol-related deaths and arrests related to drunkeness
§ Overall use dropped, but deaths spike
§ Suggests that when there is demand for a particular product, trying to prohibit it at a large scale will be problematic in driving the product underground, making it more dangerous
§ Cannabis
§ If cnnabis did have strong links with particular problems, the legalisation would show a dramatic spike in cases of schizophrenia
§ There has been increased use in the US since legalisation (maybe due to reporting - people are more likely to report it if it’s legal),

300
Q

Explain the controversy surrounding the association with substance use disorders and other mental health issues

A

People who have substance use disorders have a much higher rate of many different mental health issues compared to the general population
Personality disorders are 18 times more likely
Bipolar and schizophrenia are 11 times more likely
So there is an association between substance use disorders and other mental health issues, but the pattern is very unclear
Can exacerbate each other
Cannabis and psychosis
There is some suggestion that there may be a causal relationship
People who use cannabis regularly and heavily may develop psychosis, but this data is not experimental
However, more recent data has called this issue into question
Could be a diathesis-stress situation: people who are at elevated risk, when exposed to cannabis may increase their likelihood of being pushed above the threshold
® Very unclear whether the drug is doing this on its own or whether the individuals are developing symptoms in the first place

301
Q

Describe gambling disorder

A

• Some people view them as a pure form of addictive disorder because there’s no physiological response
• Criteria are modeled after other SUDs and mimic:
○ Tolerance
§ Need to gamble larger amounts for same thrill
○ Withdrawal
§ Restlessness/irritability when trying to cut down
○ Loss of control
§ Repeated unsuccessful efforts to control, lying etc.

302
Q

What is the epidemiology of gambling disorder?

A

○ ~70% of Australians have participated in some form of gambling over the past year
§ One of the highest rates of any country
§ Perhaps due to little amounts of regulation
○ Estimates suggest that about 1% of general population meets criteria, with 4% at risk
○ Across countries there is some variability, with a range of about 1-5%
○ In countries where gambling is not heavily regulated (eg AUS), rates are higher than countries where it is regulated (eg USA)

303
Q

What is the aetiology of gambling disorder?

A

○ Gambling machines typically operate on a schedule of intermittent reinforcement
§ This is the strongest type of behavioural learning
○ There are undoubtedly neurobiological, cognitive, and personality factors that contribute as well, but the main focus is the learning pattern