Clinical Psychology Flashcards

(159 cards)

1
Q

Enlightenment and ‘Madness’ attitudes

A

Church and its values shaped the approach that people’s roles in society starts to be judged upon.
Attitudes towards “free range” social deviants and the ‘insane’ changes with enlightenment (mid 1700s) and a new attitude towards idleness.
Started to confine those that were morally wrong e.g., those idle or those unable to reason. Madness put together with prisoners and social wider class.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

County Asylums Act (1808)

A

First mental health legislation in the UK
Required count authorities to provide for the care of ‘pauper lunatics’ so they could be removed from workhouses and prisons.
Buildings made to house the ‘lunatics’ that were originally called ‘inmates’.
Medicine at this point practically non-existent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Lunacy Aact (1845)

A

Asylum = place of refuge.
Asylums created as places of safety for the mad and poot.
Act changed the status of the mentally ill from ‘inmates’ to ‘patients’ - growing assumption that madness was a treatable disease. Increased attention paid to types of madness. Medics inhabiting these areas and, as medicine started to rise, started classifying things.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Classifying Mental Illness by the 1850s

A

By the 1850s, there was a broad agreement on the division of ‘psychiatric codnitions’ into:
* Neuroses - disorders affecting mood and self esteem - associated with fear, anxiety and panic
* Psychoses - disorders affecting reason and the indiviudal’s grasp of reality - associated with delusions and hallucinations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Who is Emile Kraepelin?

A

German psychiatrist known as the father of taxonomy of mental illnesses. He studied experimental psychology with Wundt and revolutionsed the taxonomy of ‘Madness’
His broad defintiions of these types of mental illness are enduring ever since

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Impact and general message of Kraepelin’s Taxonomy: 1889-

A

Prior to this taxonomy, people were characteristed by symptoms
However, he emphasises that syndrome (Symptom patterns) rather than single symptoms in the classification of mental illness so he could discriminate between disorders.
This brought attention to different types of disorders, bringing a step forward.
He produced an enduring taxonomy of conditions and influenced the style of all subsequent psychiatric nosologies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Psychoses and the “Kraepelinian Dichotomy”

A

Refined the separation of neurotic and psychotic condition but divided the psychoses into demential praecox and manic-depressive illness
This division was subsequently reformulated(but using essentially the same syndrome) as SZ and bipolar disorder
This was never done before, always previously put together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Kraepelin and Neuroses

A

In the Kraepelin scheme, non-psychotic mental disorders (the ‘‘neuroses’) included:
* Obsessive-compulsive disorder
* Impulse control disorder
* Anxiety disorder
* Phobias
* Hysteria and “conversion” hysteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

DSM-3 (1980)

Diagnostic and Statistical Manual of the APA - 3rd edition

A

DSM-1 and -2 are attempts to refine mental illness and classification of it further but DSM-3 considered the first manual.
Radical revision of -2 by APA (American Psychiatric Association)
Lists condition regarded as mental disorders which adopts the Kraepelinian schema and forces scientific attention to the different disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Psychiatric treatments for psychoses (to c1950)

A
  • Hospitalisation (and restraint) - in asylums
  • Coma (Insulin shock therapy, fever, ECT-induced convulsions) - idea that putting in coma or giving fever or shock will ‘reset’ them in some way
  • Sedative drugs (paraldehyde, barbiturates, etc) -high possibly of overdose
  • Psychosurgery (lobotomy, leucotomy) - very popular and dont a lot on women who weren’t very obedient to their families
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Psychiatric treatments on neuroses (to c1950)

A
  • Psychodynamic therapy
  • Hypnosis (Mesmer, Charcot)
  • Surgery
  • ECT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Issues with psychiatric treatments to c1950

A

Often ineffective.
What was effective was probably just due to chance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

The Psychopharmalogical Revolution and it’s the impact of psychopharmacology

A

In the 20-year period 1945-1965 the introduction of effective drug treatments transformed live.
Before this psychiatry didn’t offer much, but it medicine overall, this period was really important and it immensely improved the credibility of psychiatry ina way that was unprecedented.

Impact: It led to a huge decrease in psychiatric hospital care. Benzodiazepine anxiolytics were introduced in 1960 and between 1970-1980, they were the most commonly prescribed of all drugs. “Each day about 40 billion doses of benzodiazpeine drugs are consumed throughout the world” (Tyrer, 1980).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Psychopharmacology

Some of the drugs used

A
  • Lithium: Bipolar disorder (1948)
  • Phenothiazines: SZ (1953 chlorpromazine as ‘Largactil’)
  • Tricylic antidepressants: depression (1958 imipramine as ‘Tofranil’0
  • Benzodiazepines: anxiety (1960 chlordiazepoxide as ‘Librium’; 1963 diazepam as ‘Valium’) - replaced the barbiturates. Need to take loads to overdose, so improved safety. As well as effective, also safe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

After Psychopharmacology

A

Growing realisation of problems with ‘psychotropic’ drugs e.g., dependency
Physical and psychological side effects to phenothiazines
Issue of addiciton and withdrawal problems for benzodiazepines. Also, behavioural and cognitive impact if been on it for a while alongside massive overprescribing which was essentially poisoning patients and causing problems over time such as Parkinson’s. All of this for something which still isn’t a cure. Been a controll because not a cure, because manic comes back when off the drugs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Psychology and mental health

What was going on with psychology was psychiatry had its revolution?

A

Psychology (1945-) also extending theory and practice in mental health, making important contributions to:
* Assessment and psychometrics - lots of personality assessments and IQ
* The understanding of neuroses and anxiety
* Therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

The Boulder Model

A

After 1945, both the APA and BPS moved to establish ‘clinical psychology’ as a formal healthcare profession
The APA ‘Boulder Conference’ recommended a scientist-practitioner training model
* Huge milestone as looking at treatments away from emdicing
* Model still endures in the UK today
* Clinicians must get and use their practice to create hypothesis to carry through scientific methods and so on. Supposed to practice and generate science; to continuously redefine their own paradigms in their science.
* APA ‘Boulder’ model (1949) epmhasises 3 roles for clinical psychologists: diagnosis, research, therapy. Therapy meaning the psychodynamic (Freudian) therapy which was very predominant at the time, though US embraced it differently than the UK as the UK had more pragmatic attitudes towards adopting therapies than other states did.
* Althought, whilst this model was generally accepted in the UK and US, the role of the psychologist was not

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What did Han Eysenck think about Freudianism?

A

“spurious orthodoxy”
* Eysenck emphasised clinical psychology’s key role in assessment (diagnosis) and research
* Eysench wanted psychology to be like a research arm of psychiatry. Thought psychologists really good at doing research, and wanted them to continue doing that.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

UK developments

A
  • 1957: Institute of Psychiatry (King’s College, London) commences a programme of training in ‘Clinical Psychology’. Courses grow at a rate of about 1/year but no agrred curriculum
  • 1966: a BPS ‘Division of Clinical Psychology’ (DCP) formed; syllabus for a Diploma in Clinical Psychology developed
  • 1981: British Journal of Clinical Psychology launched
  • 1990: BPS/DCP agreed that all Clinical Psychology training should be 3 years (to doctorate) by 2000
  • 1995/96: First Doctoral programmes in Clinical Psychology accept students
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Developing role of the scientist-practitioner

A

1945-1970: Early role of UK clinical psychology dominated by assessment and research (IQ and neurological integrity, personality and deviancy, anxiety and depression, cognitive styles)
Little contribution to ‘therapy’
Eysenck’s (1949) view of the clinical psychologist within the psychiatric MDT: “The psychiatrist responsible for therapy, the psychologist for diagnosis help and research design, the social worker for investigation of the social consideration”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Relaxation

A
  • The method of ‘Progressive Muscle Relaxation’ introduced by Edmund Jacobson (1929)
  • Based on research into muscle tension in mental (anxiety) states
  • Amplifies the experience of relaation, modifies the experience of anxiety
  • Developed a set of instructions that were directionaly actionable and his PMR is still part of some CBTs such as for insomnia. Asked to tense muscle then relax. When relax muscle, you experience relaxation. Important because gave psychologists a tool with which they could rpactice certain parts of their therapies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Revolution in talking therapies
Psychoanalysis
Cognitive and behavioural talking therapies

A

Talking therapies popularised by Freud who was impressed by Breuer’s approach to the treatment of ‘Anna O’ who was encouraged to talk about her experiences
Studies on Hysteria was publiched in 1895, and Freud eventually developed the approach as ‘Psychoanalysis’
Eysenck regarded Freudian therapy as ‘unscientific’ and resisted its introduction into UK clinical psychology. But he became a champion for psychological therapy and evidence, evidence being what Freud;s theories lacked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Rational Emotive Behaviour Therapy (REBT)

A

Albert Ellis (1959)
Human distress doesn’t arise because of ‘unfortunate’ events and circumstances
…it arises from irrational and dysfunctional thoughts, feelings and beliefs attributed to those events and circumstances
* Emphasised the “A-B-C” model of distress
* A - Adversity (adverse circumstances)
* B - Beliefs (about these circumstances)
* C - Consequences (emotional distress when B is negative
REBT helps the client challenge and dispute the A-B-C relationship through argumetn and ‘testing’ evidence. Elements of this still form the basis of CBT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Systematic desensitisation

A

Joseph Wolpe
First to use principle of classical/operant conditioning to treat anxiety states - phobias - developed behavioural approach to anxiety disorders.
Published ‘The Practice of Behaviour Therapy’ in 1969 where he merged the conditioning concepts with PMR.
* Reciprocal inhibition: Learn a new response to the phobic stimulus which inhibits (i.e. is incompatible with) with anxiety: e.g., learn to RELAX in the presence of phobic stimuli
* Systematic desensitisation: Practise the new response at each level of a graded exposure to the phobic stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Cognitive Therapy
**Aaron Beck (Father of Cognitive Therapy)** * How we think about a situation determines how we subsequently feel about it * Typical patterns of thinking = 'cognitive schemas' * Cognitive schemas can be realistic and adaptive, or 'negative' * Negative schemas can become ‘automatic’. producing habitual negative emotions * Negative schemas are characterised by cognitive bias - cognitive ‘errors’ or ‘distortions’ * Addressing cognitive errors directly by cognitive reconstruring which is challenging a negative schema and replacing it with postiive or realistic alternatives. Or addressing errors indirectly by distraction or blocking strategies which prevent negative schema formulating
26
Cognitive and Behavioural Therapies Morphing 'CBT': 1980 - 2000
Different theoretical origins but: * This gave soemthing measurable, simple and achievable * Both 'symptomatic', psychotherapies (non-exploratory) - target those symptoms very specifically * Both suited to ‘brief intervention’ models (4-8 clinical sessions) - very quickly, a manual was developed * Both effective in the treatment of mental AND physical health problems - started to be noted a lot of mental health accompanied with physical health issues such as pain * Both enthusiastically adopted by clinica; psychology in the 1980s Morphing: * CBT: The pragmatic combination of Cognitive and Behaviour Therapies * From a treatment delivery perspective, more similarities than differences * Fusion supported by evidence of efficacy * Lot of forms of CBT use cognitive therapy.
27
3 major reviews on clinical psychology in the NHS
1. Trethowan Report (1977) 2. The Management Advisory Services Report (1989) -- psychologisys have equal status as medical practitioners 3. The Manpower Advisory Group Report (1990) All 3 establish clinical psychology as an independent profession, not an arm of psychiatry. The Mental Health Act (2007) amended the 1983 Mental Health Act making those in charge of patient treatment changed from ‘responsible medical officer’ (RMO) to ‘responsible clinician’ (RC). CPs can now head the team in care of a patient. RC doesn't need to be a consultant psychiatrist, but an approved clinician (AC). With appropriate training, clinical psychologists are eligible for AC/RC roles
28
The Science-Practitioner Role | What is "Evidence Based Practice" (EBP)?
From the early 1980s UK CP has consolidated 3 distinctive roles: Assessment; Therpay; Research. The role consolidation supported by the development of EBP - using the best available evidence in deciding whether a given treatment works, and for whom it works. Which of the 2 (or more) treatment options are more effective and affordable? Both decides on efficacy of a treatment, which means does it work? Affordable is still a highly important principle when in a healthcare system. - Commits clinical psychology to an ongoing programme of controlled outcome assessment - Makes psychological therapies a continuing ‘work in progress’ - Roth and Fonagy’s (2004) “What works for whom?” provides a landmark in evidence synthesis
29
NICE
*National Institute for Health and Care Excellence* founded in 1999 as an arm of the Department of Health * Using methods of systematic review and evidence appraisal, NICE aims to improving health and social care through evidence-based guidance * When presented with treatment, need to look at evidence and if there then appraise it to see what is the level and quality of evidence to suggest this treatment if efficacious or effective. * These authoritative outputs are often referred to as “NICE Guidelines” * NICE guidance has become very influential in determining which therapies are appropriate (and which therapies) should be commissioned) within the NHS * As a scientist-practitioner enterprise, clinical psychology both generates evidence and adjusts clinical practice in line with results
30
DSM-5 vs ICD-11
ICD-11 used a lot in Europe and England. DSM-5 used more in US and research. ICD-11 is the manual of the World Heal Organisation
31
DSM-5 Major Depressive Disorder
Five (or more) symptoms in a two week period, representing a change from previous functioning *(distinguishing from those more miserable generally)*, in addition to either depressed mood and/or loss of interest or pleasure (anhedonia): * Significant weight loss or gain * Insomnia or hypersomnia * Psychomotor agitation or retardation * Fatigue/loss of energy * Feelings of worthlessness and/or guilt * Diminshed ability to concentrate or indecisiveness * Suicial ideation
32
Culture and symptoms - Haroz et al. (2017)
62% of patients endorse symptoms of DSM-5. But others no captured by nosologies. Looked at large sample and cultures. Found common amongst both Western and non-Western cultures Socialisation or loneliness was 4th most endorsed symptom of depression. More than half endorsed that as significant symptom. But not really included in DSM-5 * Social isolation/loneliness * Crying a lot * Anger * General aches and pains * Headaches * Thinking too much
33
Prevalence of depression
(WHO, 2021) * 5% of the world’s population, with prevalence steadily increasing - *maybe says something about effectiveness of existing treatment or the environment around us* * Ranked as the single largest contributor to non-fatal health loss (7.5% of all Years Lived with Disability) * Most prevalent in low- and middle-income countries * 2:1 female to male ratio * Comorbid with anxiety - *With something but a lot is comorbid with anxiety*
34
Consequences of major depression
* Cognitive functioning - most severe forms indistinguishable from dementia * Occupational functioning - lack of energy, inability to concentrate means a lot of the time people stop working or show up but contributing little * Social relationships - tendency to be anrgy, egocentric. When in pain, focus on own pain so difficult to maintain relationships around you. Divorce more prevalent amongst those groups * Suicide - mortality doubles independent of mental health disorders. Other ways in which life shortens too, not only suicide. Might affect self-care, adherence to medication, other disorders. Independent of depression, does shorten life
35
Biological aspects of MD
1. Symptoms (e.g., lack of energy, appetite disturbance, sleep disruption) indicates malfunction of overall system 2. Depression runs in families (suggests genetic link though could just be because exposed to the symtpoms, not necessarily biologically programmed) 3. Brain imaging (e.g., PET, fMRI, MRI) of functional changes to the brain such as hippocampus and amygdala. Size of brain may change and therefore functions affected. 4. Changes in NT and hormone levels (e.g., serotonin and dopamine) 5. Success of biological treatments in treating MD (e.g., antidepressants, ECT)
36
The Monoamine hypothesis
**Pathophysiologic basis of depression - depletion in the levels of serotonin, norepinephrine, and/or dopamine in the CNS**. A significant proportion of patients with MDD are resistant to monoaminergic antidepressant therapies. Led to development of anti-depressants. Tricyclic originally unsafe but got safers and started targeting different NTs. But issues as anti-depressants treat everything (Depression, OCD, whole class which are meant to be discrete and different disorders which come from different malfunctioning of brain) so problematic that they target all of these disorders. Alsoproblematic because not a response to most patients. Most patients of depression do not respond to anti-depressants. STAR*D trial - 1/3 of patients achieve remission with initial antidepressant pharmacological treatment
37
Early psychological models of depression: Reinforcement theory | REBT is also one
Reinforcement theory: Charles Ferster 91973) functional analysis viewed depression as a generalised reduction of rates of response to external stimuli. Withdrawal from environment but because lack of stimuli. Theorised depression happened as response of loss to that due to life events e.g., loss of job or significant relationship, transition such as moving to university. Lewisohn (1974) develops this as depression as a response to insufficient response-contingent positive reinforcement, to maintain adequate functioningg. Made more complex as added some cognitive factors such as a lack of skill within individual to respond to that lack of stimuli. Maybe social skills not developed enough to develop other relationships. Called them poor inter-personal skills Interfering anxiety: theorised that was a very significant factor in way respond to loss of external stimuli Comes a point when experience this loss and is so significant that you tip into depression and coping mechanisms no longer functioning adequately to respond to that.
38
What did the reinforcement theory lead to?
Positive Reinforcement and Behavioural Activation * Psycho-educational approach (“The Coping with Depression Course” (Lewisohn, Antonuccio, Breckenridge, & Teri, 1987)) - Initial took form of pleasant events life schedule. Treatment initially a list of things you could engage in which could widen your experiences in order to receive those positive reinforcers back. * + negative reinforcers: Behavioural Activation (Martell et al., 2001) - Do things that negatively reinforce your depression. People who reinforce symptoms and don’t make it better. Not sufficient enough to increase positive experiences, but need to deal with negative reinforcers through e.g., avoidance, therapy etc. * + matching theory: Behavioural Activation Treatment for Depression (Lejuez et al., 2002) * takes into account that reinforcers, postitive and negative can be individual, what works for one doesn’t work for others. Need to match the stages. This has increased in complexity as went along, starts with pleasant event then make it more complex to look into more complex circumstances. Proportionality of positive and negative reinforcer is to be taken into account. Matching theory looked at proportionality of positive vs negative reinforcers and trying to match it
39
Cognitive theory of depression
Beck (1972) * "Cognitive triad" of depression: a negative view of self, worlf, and future * Schemata: structural units of stored information that also function to interpret new experience * Latent depressive schemata reactivated when loss is perceived - Problem of depression is located in the head of the individual, not in the environment. Still the thought today * Cognitive distortions * Theory led to therapy which focused on making interpretation of events rational and realistic by focusing on beahviour, automatic thoughts, and underlying assumptions. Highly efficacious to depressed patients, with positive effects maintained over the longer term (deRubeis & Beck, 1988; Dobson, 1989; Rehm & Kaslow, 1984; Williams, 1984). * Highly influential in CP, and valuable in applications like CBT.
40
Cognitive distortions types
* Arbitrary Inference - The arbitrary assumption that some negative event was caused by oneself * Selective abstraction - Focus on the negative element in an otherwise positive set of information * Magnification and minimisation - Overemphasising negatives and underemphasising positive * Inexact labelling - Giving a distorted label to an event and then reacting to the label rather than to the event ...leads to automatic thoughts
41
Anxiety vs fear
* Highly correlated, but separate concepts * Anxiety: Concern about a perceived future threat * Fear: Response to a perceived immediate threat * Anxiety and fear responses involves physiological arousal via the sympathetic nervous system
42
Is anxiety "normal"? | State vs trait
Anxiety serves a purpose: promotes the fight or flight response, which is adaptive * State anxiety: Response to a particular situation High and maladaptive: Acute Anxiety * Trait anxiety: Range of anxious responses related to personality structure High and maladaptive: Chronic Anxiety State happens in the moment. Trait is related more to personality structure
43
Symptoms of anxiety
* Psychological arousal * Sleep disturbance * Muscle tension * Autonomic arousal * Hyperventilation Understood to be more of an embodied experience than depression. Heart rate increase, muscle tension, quite immediate physiological response
44
Prevalence of anxiety
* Lifetime prevalence around the world ranges from 9% to 29% * More common among females than males * 6th largest contributor to non-fatal health less globally and appear in the top 10 causes of YLD in all WHO regions * Disabling disorders with high impact on day to day functioning: social isolation, homebound
45
Aetiology of anxiety disorders
Dimensions: biological, sociocultural, social, psychological (diagram in notes) * Amygdala: key role in formation of emotional memories. Those with high anxiety, there is a dysfunction in amygdala and is hyperresponsive, and neural dysfunction in the hippocampus. Alerts hippocampus and prefrontal cortex. 2 pathways: short route for immediate threat. Long route when perceived threat is appraised by cortex. Hypothesised that people with anxiety has bias of appraising stimuli through short route. * GABA: inhibitory NT with big role in moderating other NTs and influential in how work, but also number of receptors associated with stress in environment. Those with anxiety has lower levels of GABA. Benzodiazepines bind to GABA(a) and facilitate GABA, reducing neuronal excitability
46
Intolerance of Uncertainty (IOU) | Dugas and Koerner (2005)
Individuals with GAD find uncertain or ambiguous situations to be stressful and upsetting, resulting in chronic worry and anxiety about these circumstances * Not really about appraising a stimulus being fearful or not, but being faced with something and how you don’t know if it will be fearful or not. It’s those uncertain situations provoking the anxiety. * Most situations are uncertain. Hard to beforehand control or anticipate everything you encounter in life and classify as fine or not fine. Beliefs that that worry will serve to either help them cope with feared events more effectively or to prevent those events from occurring at all. * Worry is seen by people with anxiety as a positive thing. Helps them with coping about what’s coming. ‘If worry, then can think and anticipate what will happen which if of value so I can prepare myself’. Worry seen as positive reinforcer *Anxiety becomes a disorder when threats or dangers are seen where they are not really present, the physiological response to anxiety occurs, and the behavioural responses of avoidance, escape and use of safety behaviours perpetuate problem
47
Define: aovidance; escape; safety behaviours
* **Avoidance** is when individual does not put themselves into the feared situation * **Escape** is getting out of it * **Safety behaviours** are things the individual does whilst in the situation to help them to deal with it. Gives people a sense of control in the situation they find themselves in
48
Generalised Anxiety Disorder (GAD) - DSM-5
The presence of excessive anxiety and worry, which occurs more often than not for at least 6 months Associated with: Edginess or restlessness; Impaired concentration; Irritability; Difficulty sleeping *Adult worries include job responsibilities or performance, health, financial matters and other everyday, typical life circumstances. Child worries is likely about abilities and performance.
49
Intolerance of uncertainty model | More depth
* Anxiety leads to negative problem orientation and cognitive avoidance, both of which serve to maintain the worry * Negative problem orientation: lack confidence in their problem solving ability; perceive problems as threats' become easily frustrated when dealing with a problem, and; pessimistic about the outcome of problem-solving efforts (Koerner & Dugas, 2006) - these feelings servce to exacerbate their worry and anxiety * Cognitive avoidance: Use of cognitive strategies (e.g., distraction, thought suppression) that facilitate avoidance of the cognitive arousal and threatening images associated with worry * IOU scale: Prospective Anxiety (not yet happened but anticipate it, examining everything about a situation that's about to happen) and inhibitory anxiety (inability to act in prsence of anxiety, usually free or avoid response) * IOU scale found to predict symptom severity (Dugas et al., 2007). The model’s primary focus is on cognitions as the key component that drive the development and maintenance of GAD
50
The tri-partite model (Clark & Watson, 1991)
* Physiological hyperarousal (anxiety) * Low positive affect (depression) * Negative affect (shared) *Theorised a shared element in all mental health disorders of negative effect* Non-specific general negative affect factor shared by other disorders (e.g., psychosis; Wilson et al., 2020) - important transdiagnostic factor
51
Evaluation of cognitive models of GAD IOU - Transdiagnostic factor in emotional disorders?
Individuals with GAD and OCD experience greater degree of intolerance of uncertainty than non-anxious controls, with no difference between GAD and OCD groups (Holaway, Heimberg, Coles, 2006) - *Noticed that as a concept, IOU was present in other disorders too to an extent. Presence of the concept as measured with the scales we administer was present in other disorders too such as depression. * * High comorbidity between GAD and MD, anxiety likely to appear first. * MD and GAD found to share a single genetic diathesis * Seems to always precede the onset of other mental health disorders - see the hierarchy. * When experiencing stressing events, we externalise that but eventually it goes into an internalising experience of this. - hierarchical model with two broad factors: internalising and externalising. * Internalising factor (distress.misery for MD and GAD, and fear for phobias and panic disorders) seems to lend itself better in explaining depressive symptoms and externalising factors in those in the way we manifest those experiences, which seem to pertain mostly to anxiety disorders.
52
Ways of measuring sleep
* The Actigraph is the most widelyused measure of sleep which relies on the fact that you should be immobile when asleep. Data shows on an actogram. * Polysomnography looks at brain activity. Electrodes are put on the head and face to see the electical activity of different muscle groups to see which stages of sleep the person is in, and these signals are converted into data. * However polysomnography can be accompanied by a small margin of error due to interpretation. It also relies on expertise and is time-consuming so nnot widely used.
53
Measuring the depth of sleep | What does the hypnogram show?
The 'Auditory Arousal Threshold' * minimum amount of nosie required to arouse someone from a given stage of sleep. * The 'deeper' stage requires more noise (and energy) * Different stages of sleep means different levels of consciousness. * The hypnogram shows that the deeper stage of sleep is taken during the first part of the night. Evolutionary? The body is biased to get it over with and gets lighter and lighter and progress through morning. Perhaps because body gets the essential part done with.
54
Sleep is controlled by 3 processes. What are these?
Homeostatic, circadian, and psychological
55
Homeostatic process of sleep
Physiological balance * Adenosine (NT) increases once awake, hits peak (After about 16 hours) then body needs rest. With sleep, adenosine is dissipated, then the cycle starts again when wake up. * Physiological process in brain inducing sleepiness * If acculumate sleep deprivation, will make up for it. Sleep pressure best illustrated where children will fall asleep reagrdless of where they are. Learn to overcome in adults such as drinking coffee (which antagonises adenosine). Learn to control sleep pressure to an extent, but the process with eventually win, no matter what
56
Circadian process of sleep
Biological internal clock * Entrainment of 24 hour cycle mediated by non-image forming retinal cells (intrinsically photosensitive retinal ganglion cells or ipRGCs) * Through light that falls on retina, tells brain you should be awake. In time, trains body to be in sync with your environment. * Rhythm still works without the light. Roughly follows same pattern of activity and rest. Those blind to light, system not entrained to day and night and deal with this through medication like melatonin * irRGCs link directly to the suprachiasmatic nucleus in the pineal gland * Light suppresses melatonin secretion, which rises in darkness * Homestatic and circadian processes work together to create perfect timing and conditions for you to sleep. Upon waking, process C ensures you are alert, temperature is high and adenosine is low. Creates consolidated period of wakefulness that promotes waking activity cause cognitive alert and all the physiological processes help you to be alert. Critical point in both of them where need rest. Cognitive function compromised to significant level after 16 hours.
57
Psychological process of sleep
Learning; cognitive arousal; automaticity * Control of sleep onset * Psychological conditions influence sleep onset and control of going to sleep. Insomnia about the control of sleep onset. * Sleep onset most probable when: appropriately sleep; go to bed at appropriate time; appropriately calm; sleep environment is familiar and assocaited with restfulness * *First two about physiology. First is homeostatic. Second important for circadian process. Calm - control cognitive arousal*
58
Epidemiology of Insomnia
* >10 million prescriptions for hypnotic drugs issued in NHS primarycare/year * Women suffer more than men * Insomnia is the most prevalent sleep disorder. Symptoms can be very high, especially in student population (about 63%). Probably mirroring the increase in other mental health problems too. Similar across the world, roughly stable acrss the world * Trend in women vs men holds across cultures, increases with age. Not suprising given that a host of physiological processes that happen with aging that create favourable conditions with insomnia e.g., increased having to go to the toilet at night, menopause. * Prevalence: Hartescu and Morgan (2019) found highly prevalent in UK and south africa, lower in china compared to other countries so know must be some cultural component in way people complain and understand their sleep
59
Insomnia and co-morbidity
* Insomnia symptoms are within other mental health problems such as major depression, GAD, panic disorder, PTSD, OCD * Before 2005, insomnia had two categories: primary insomnia (insomnia with no comorbidity) and secondary insomnia (insomnia resulting from comorbid conditions) * However 2 strong arguments against "Secondary insomnia" (Outcome Evidence Synthesis, 2006): CBT-1 effective in secondary insomnia too, and insomnia often continues after the presumed primary disorder has remitted
60
Insomnia Disorder (DSM-5, 2013) and its consequences
* At leat 3 times/wk for at least the previous 3 months of persistent complaint of difficulty initiating or maintaining sleep, despite adequate opportunity to sleep, which causes significant distress, and is associated with impaired social or occupational functioning. * Consequences are: chornic fatigue (fatigue is won't sleep if put head down, with sleepiness you will); emotional dysregulation; cognitive and psychomotor impairment; increased accident risk; delayed recovery from acute illness episodes; increased accident risk; delayed recovery froma cute illness episodes; increased healthcare utilisation; increased litearture of those committing suicide having a period of insomnia before; independent risk factor for other mental health conditions as can be a predictor of future: depression, anxiety, -OH abuse, and possible psychotic symptoms (Hertenstein et al., 2019)
61
Assessing sleep quality
Difference between insomnia and healthy sleep is the complain that somebody engages in. Distress and loss of function they complain about etc. So ask simple question of do you have problems getting to sleep Insomnia affects about 10% of the population. Everyone experiences sleep disruption at some point in their lives, but only a minority develoop chronic insomnia
62
Spielman "3P" model of insomnia
* Very powerful as lot of research supporting it. Also explanatory and makes sense to those who don't understand sleep much. * Predisposing factor: maybe genetic, trait, environment that predisposes you to develop certain disorder. People with insomnia can be characterised by a behavioural phenotype showing: attentional bias, higher trait anxiety, and a propensity to ruminate/catastrophise. * Precipitating factor:life event happens that creates some acute insomnia symptoms. E.g., stressful presentation to prepare, childbirth, illness. * Perpetuating factor: Maybe because sleep is continuously disturbed and you're annoyed with it, engaging in behaviouts which are counterproductive to insomnia.
63
CBT-I treatment outcomes and NICE evaluation of it
* “5 hours psychological treatment…produces reliable and lasting improvements…among 70-80% of treated patients” * No longer a question of whether it works or not, but a question now of effectiveness. * As opposed to hypnotics drugs, hard to come off because rebound insomnia occurs when come off it. * NICE TA77 (2004) says hypnotics considered only after due consideration of non-pharmacological measures. CBT-I should be considered as first-line treatment. * Research shown highly efficacious, and cheaper and better for ppts in the long term.
64
What is CBT-I and its aims?
An integrated ‘package’ of cognitive and behavioural interventions designed to: * Reduce sleep latencies (reduce amount of time to fall asleep. Gives less time to engage in cognitive arousal) * Increase sleep efficiency (Sleep efficiency is a measure of how long spend time in bed asleep. Ideally about 85%. Activities should be outside of bed as in time the bed will lost discriminatory properties of being in bed as being a place to sleep) * Re-establish stimulus control (Important goal for therapy is to pair again, and re-establish those discriminatory properties to facilitate falling asleep instead of facilitating cognitive arousal )
65
CBT-I: A stepped care model
Programms escalates intensity of treatment * Sleep hygiene (Reducing dysfunctional beliefs/amplifying circadian control. Mainly advise and reducing beliefs you don't have to sleep for 7 hours, that's just a normal distribution) * Sleep restriction (perhaps one of most powerful steps and pulls psychological leveres to train people with insomnia to fall asleep. Increase homeostatic sleep pressure at bedtime by shrinking the amount of time they can stay in bed for then extend. Theory that will fall asleep fast if only allowed short time in bed). * Stimulus control (managed wakefulness and '15 minute rule' which is if can't sleep, must get up and do something away from bed. Only allwoed in bed to sleep) * Relaxation (reduce cognitive arousal/PMR: way of blocking thoughts, or stopping that cognitive arousal) * Cognitive therapy (reduce cognitive arousal at night; restructuring - thought blocking; more about reframing thoughts, and catastrophising.
66
3 key psychologica factors are influential in the regulation of sleep: Cognitive arousal
* People with insomnia have inability to regulate mental activity. Struggle to switch off e.g., my mind is racing, I'm a worrier, I can't stop thinking. * Harvey (2002): Selective attention → monitoring: If have higher cognitive arousal at night, eventually stumble across something that worries you which creates more cognitive arousal. Said people engage in monitoring of their sleep or cues around their sleep. Notice not asleep, people with insomnia notice this and worry about it. Start monitoring everything else in their environment, internally that confirms those beliefs e.g., clockwatching. Clock monitoring not helpful and directs to monitoring behaviour that late and still not asleep. * Espie et al. (2006): Selective attention → the A-I-E pathway: Arousal --> selective attention to delayed sleep onset, compensatory intention to fall asleep, counterproductive deployment of 'sleep effort' --> arousal. Sleep effort means loss of ‘automaticity’, introduces other conscious processes which come at cognitive and time cost. Sleep effort generates performance anxiety and LONGER sleep latencies. Fall asleep best when don't try to sleep. But, if chronic, arousal-delayed sleep onset can impact learning processes. Impacted by repeated arousal delayed. Because everything learned through conditioning can be unlearned. Compensatory intention - once established not asleep, then want to fall asleep and attention is particularly bad. Once deeply intention on detail of it, slower and most likely will create cognitive arousal. Idea it all starts with arousal.
67
3 key psychological factors are influential in the regulation of sleep: Learning | The other psychological factor is automaticity
* Learning (’conditioning’) can take place through: Reward/reinforcement (operant conditioning) or Pairing (classical conditioning). Both processes require behavioural repetition (’habit’ or ‘routine’). Sleep onset characterised by repetition (Type of behaviour you do everyday. Like eating) * Satimulus control of sleep: Adopting the state which leads to sleep is rewarded (reinforced) by sleep onset. Through repeated episodes of reinforcement, the bedroom acquires discriminative stimulus properties for reinforcement. Will be ahrder to sleep if use bed and room to work, eat, sleep, rather than just sleep because of the associations. Discriminative stimuli make behaviour (previously reinforced in their presence) more likely * Insomnia as an extinction programme but waht is learned can also be unlearned. Chronic insomnia extinguishes learned associations between the bedroom and sleep onset. As a result, the ability of the bedroom environment to signal 'sleep' is diminshed. * Conditioned emotional responses: repeated associations between the frustration of delayed sleep onset, the sleep environment; classical conditioning of negative emotions (conditioned arousal) on going to bed. Will be thinking ugh now i need to sleep, which brings a host of negative emotions in response to falling asleep * Stimulus control and sleep: in other words...for people with chronic insomnia, bedroom environments stop promoting rest and sleep, and start promoting cognitive arousal.
68
Definition of eating disorders
Severe, psychiatric disorders characterised by a dysfunctional relationship with food and distorted perceptions about the body, that significantly impairs physical health and/or psychosocial functioning. (APA, DSM-5). *Broad of just ED definition. E.g., doesn’t state the kind of dysfunctional relationship, but more detail in each ED listed within DSM-5.* Continuum - don't always stay in the same place
69
DSM - Anorexia Nervosa
* DSM-4: Refusal to keep body weight above minimal healthy level (85%). Fear of weight gain - perception much larger then are. Disturbance of body experience. Amenorrhea (absence of the menstrual cycle for about 3-4 months * DSM-5: Restriction of intake leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health * DSM-5 dropped 'refusal' as places emphasis on unwillingness and resistance of individual. Dropped 85% so greater felexibility on clinican to decide whether underweight. Dropped amenorrhea entirely as escludes men; menopausal women, pre-menstrual women, women on contraceptive, those still on their period * Subtypes - restricting; bing-eating/purging. If core feature is restricting, with binge-eating or purging that would be anorexia. If core feature was binging and purging, then would be assigned to a different eating disorder
70
DSM - Bulimia Nervosa
* DSM-4: recurrent episodes of binge-eating, compensatory beahviours, bingeing and compensation happen twice per week over at least 3 months, self-evaluation in unduly influenced by body shape and weight, not simply a phase of anorexia. - *binging - eating a lot and accompanied with a lot of control. Very large quantities of food, typically high fat. Compensation could be self-induced vomiting, laxative abuse, or excessive exercise behaviours* * DSM-5: same as above expect for frequency reduction. Bingeing and compensation happen once per week over at least 3 momths, not twice per week.
71
DSM - Binge eating disorder
DSM-4 released 1994, DSM-5 released 2013. * BED new to DSM-5. Was recognised before but in the residual category. * Recurrent episodes of eating significantly more food in a short period of time than most people would eat under similar circumstances; eating very fast in the absence of hunge (Eating alone; large amounts of food when not hunrgy) * Marked by feelings of loss of contol and guilt, embarrassment or disgust (same as BN, but not followed by any compensation e.g., purging behaviour. Bingeing happens once per week over at least 3 months).
72
Other specified feeding ot eating disorders (OSFED; DSM-5)
Formally known as EDNOS in DSM-4 (Eating disorders not otherwise specified) * Atypical AN * Low frequency BN (meet all criteria but just do it less, though still experiencing significant stress and impact on QoL) * Purging disorder (Just the compensating behaviours, but not in compensation for anything, no binging) * Night eating syndrome (tendency to binge and overeat but exclusively during an evening or overnight. Not during other times of the day.)
73
Other EDs in DSM-5 (not OSFED)
* Pica * Rumination disorder (self-induced regurgitation of food) * ARFID
74
Issue with sub-threshold disorders in DSM-5 (OSFED)
40-50% cases do not fit neatly into diagnoses. OSFED are the largest group Many people move from one diagnosis to another Sub-threshold most common So small amount getting treatment as most put into OSFED or broader disordered eating category
75
Incidence and prevalence of EDs
* 62% of people with EDs have symptoms before age of 16. Though, all figures from Westernised cultures. * Peak age of onset slightly younger for AN (14-16 vs 18-20) * BED - more common in males and older people. Most equitable in distribution between males and females. * Female:male ratio 20:1 roughly, but more recent suggestions are 10:1. * **Prevalence**: (number of case in population at any time) AN - 0.5-1% of teenage girls, BN - 1.2% of women aged 16-35. BED - Lack of epidemiological studies but estimates of 3.6% of women, and 2.1% of men aged 18-70. OSFED - 2-3% of women aged 16-35 * **Incidence**: (number of new cases in a year) AN - 21 new cases per 100k population. BN - 30 new cases per 100k population. BED - not known yet, similar to BN?.
76
Why might prevalence/incidence rates differ?
* Definitions used for diagnosis - DSM-IV vs -5. * Individual assessors/therapist opinion * Sample - clinical cases only or self-reported. Eating disorder questionnaires not considered as gold standard as clinical assessment of it * Other research variables e.g.,s new cases only, not re-referrals (which are quite common in EDs) * Across cultures; less ED? Less acceptable? Fewer treatment opportunities?
77
COVID-19 and EDs
* Systematic review of 53 studies (Devoe et al., 2022) * Evidence to suggest that the pandemic led to: increased diagnoses of EDs (↑15%); increased hospital admissions for EDs (↑48%); and increased ED symptoms. * Increased co-morbidity (e.g., anxiety, depression, suicidal ideation; Taquet et al., 2021) * Decreased access to care and treatment, changes to routine and loss of structure, social isolation
78
Issues with diagnosis and treatment
One average it takes 15 months between spotting symptoms and starting treatment Hamilton et al. 92022) - 5.28 years between symptom onset and treatment seeking in Australian sample (n=119) * Potential causes of these delays: denial they have a problem or need support; concerns over stigma; understaffed; limited access. * Gilbert et al. (2012) found that the more positively disclosures were appriased, the quicker the subsequent help-seeking.
79
Costs of EDs
EDs now cost the UK £15b a year NHS: 60% of costs are for females under 24 years; £510 per day per inpatient; outpatient costs are about 40% of inpatient; GP visits; treating associated problems (e.g., BN affted dental health) Also costs to employers and government
80
Premature death and disability-adjusted life years of EDs
Premature death: Those with ED 5x more likely to die. Meta-analysis from Arcelus et al. (2011) found that BN has 1.7 deaths per 1000 patients, AN around 6, 3.3. for OSFED. Disability-adjusted life years: EDs are 6th in terms of DALY from early mortality and reduced quality of life for ages 15-24.
81
Risk factors of ED
* Female; adolescent/young adult; sociocultural pressures and expectations "thin ideal" * Biological: genetic predisposition;serotoning dysfunciton * Family history of: depression; substance/-OH abuse; eating disorder; obesity; chronic dieting * Experiences: parenting (invalidating environment); abuse; critical comments regarding eating, shape and weight; presures to be slim e.g., lean sport, ballet, gymnastics * Individual characteristics: low self-esteem; perfectionism; anxiety problems; obesity; early menarche
82
Genetic model of ED
* Eating disorders appear to run in families. * Strober et al (2000): female relatives of AN patient x11 more likely to develop AN. * Some specificity for ED type; but risk for all EDs is higher among first degree family members. * Heritability estimates up to 0.74 for AN * 55% identical twins concordant for AN. * Much weaker for BN (less is known about the genetic pathways for other EDs). * Significant genetic correlations between AN and other psychiatric disorders (e.g., schizophrenia); Some overlap with genes identified as potentially problematic in EDs with SZ. * Large genetic studies identified certain patterns of genes that seem to be important. Not one single gene identified
83
Neural model of ED
Brain chemistry being different. Researchers focused on AN. Suggested lower levels of serotonin in guiding food regulation. Idea those with AN more able to restrict food intake because don’t have same food hunger experiences as everyone else. Don’t experience same drive and compulsion from rest of general population. * AN may have lower levels of chemical in brain that might be involved in intake regulation * I.e., do not feel hungry and so do no eat
84
Psychodynamic model of ED
Way of understanding patients' experiences * Emphasises meanings atached to symptoms and function to them (Restriction = success / personal effectiveness / avoidance of sexuality (Bruch, 1974); Vomiting = rid oneself of traumatic sexual experience or fantasy pregnancy; Hunger = greed (Dare & Crowther, 1995); Attaching fundamental meaning to symptoms) * Emphasise role of infancy and subsequent experiences in shaping a person (control and avoidance of maturation) * Focus on unconscious components
85
Transdiagnostic cognitive-behavioural model of ED | Look at the diagram on notion for it to be better.
* Tries to link cognitions with the behaviours that then emerge. Positions individual characteristics that feed into thoughts which result in certain types of behaviours which perpetuate some behaviours. Mood intolerance is inability to cope with negative emotions. * Aims to explain both AN and BN. Core behvaiours established via psoitive and negative reinforcement and can include cognitive state.
86
Family systems approach of ED
* Family not the cause, but context in which ED is embedded (Eisler, 1995): symptoms as communciative acts, the homeostatic family; boundaries (wtihin ED treatment with family system, setting clear boundaries is important in that therpay technique); conflict avoidance * *Perhaps family system where communication is discouraged or not possible, or negative ramifications for talking about these things, and ED becomes way of communication and impair it further. Family unwilling to discuss difficult topics.*
87
Sociocultural model of ED
* Expression of social values * Culture-bound or ethnic disorder: Gender role conflicts – traditional feminine role may be protective against ED (Silverstein et al., 1986); Japan. (See lower levels of ED when still this structure that societies where women have greater chance to identify); superwoman syndrome (Thornton et al., 1991) as expectations upon women may contribute to ED problems; identity: child vs independent (links to PD model. State of child easier to cope than being an adult; strong but look tiny; representations of beauty through unattainable levels of thinnes; evidence to suggest increase in EDs when exposed to westernised ideals (e.g., introduction of TV in Fiji; Becker, 2004; social networking; Becker et al., 2011).
88
Significant events approach of ED
* Sexual abuse: About 30% of ED patients (Connors & Morse, 1993) but may be more significant in men * Childhood loss: face validity but not supported by evidence e.g., death of parent, divorce, or other significant life events in that space
89
Co-morbidity of eating disorders (Swinbourne et al., 2012)
(Swinbourne et al., 2012) * 100 women presenting for treatment of an eating disorder and 52 women presenting for treatment of an anxiety disorder. * almost 2/3 of women presented to ED services met the criteria for at least one or more anxiety disorders. Seemed to have anxiety first, followed by subsequent eating disorder. Other comorbidities: self-harm, axiety disorders, depression (and other mood disorders), substance use, personality disorders, temporal RSs are not always clear. Rare to see and ED isolated from other disorders.
90
Treatments for EDs | more details on notion
AN focuses on reaching a healthy body weight or BMI; psychoeducation; monitoring weight and physical and mental health; enhancing self-efficacy; cognitive restructuring etc. BN focuses on establishing a regular pattern of eating; addressing eating psychopatholgoy; psychoeducation and engagement; encourages patients to go through guided self-help route BED focuses on psychoeducation; self-monitoring; daily food intake plans; coping with risks and trigger; body exposure training Remission rates for EDs are poor. Brockmeyer et al. (2018) found rates at a 1-2 year follow up for AN were 13-50%, and Quadflieg and Fichter (2019) found 30-40% for BN.
91
How does T differ from LGB?
Critique with LGBT because the ‘T’ is identity not sexuality. Some older research is actually only looking at LGB not LGBT, but improved in recent years. Different in terms of level of discrimination. Acceptance more progressed for sexuality. Difference in what is involved. For someone identifying as ‘trans’ has impact on body, surgery, hormones etc. Big impact on reaching their identity.
92
Clinical definition of transgender | ICD-10 definition
Term "trans" is umbrella. Transgender = other gender to one assigned at birth Transmasculine/feminine = a person who identifies as non-binary but leans towards the opposite sex gender expression * A desire to live in and be accepted as a member of the opposite sex, usually accompanied by a sense of discomfort with, or inappropriateness of, one’s anatomic sex, and a wish to have surgery and hormonal treatment to make one’s body as congruent as possible with one’s preferred sex * Persistent for 2 years * Not symptom of other mental disorder - Reason why people currently go through a clinical process for gender identity. Sometimes, gender identity problems can be manifestation of a different disorder. Need to be sure of what is going on. Now controversial within people seeking treatment who don’t want to have to go through this process.
93
Differences of Sex Development
People born with variations in sex characteristics that do not fit the typical definitions for XY male or XX female bodies - often no known until puberty
94
Historical context of LGBT
* 1910s/20s - Magnus Hirschfeld made the disctinction between a desire of others of the same sex (LBG) and a desire to live as someone of a different sex (T) than that assigned at birth * 1965-1978 - Both appear together in the ICD-8 (1965), the ICD-9 (1975), and DSM-II (1978) as sexual deviations * 1960s onwards - Harry Benjamin popularised the term transsexual, distinguished from transvestite, and advocated for healthcare needs
95
Transgender terminology...and problems
* Until recently, common terminology was: Mtf or FtM (male to female and female to male) and natal male or natal female * These were somewhat problematic and so replaced with: birth-assigned female (BAF) and birth-assigned male (BAM) * Now replace again with: assigned female at birth (AFAB) and assigned male at birth (AMAB) * Problems as suggests deviation from normal and stigmatisation
96
Binary bell curve and heteronormativity
* Live in binary culture but argued we are on spectrum from very masculine to very feminine. Cultural influence that causes this double bell shaped curve that pushes people into these groups. Sport perpetuates differences and very influential in upholding the gender binary. Only now starting to fund women playing football * Heteronormativity is the assumption by society that everyone is heterosexual, and cisgender. Butler (1999) shows the dominant view of a fixed sex which culture builds a stable gender to determine your desire (opposite sex). But should have alternative view of fixed sex and you perform an identity and you may have desires. * Because lot of diversity at many levels as table in notion will show. Differences in chromosomes, hormones, puberty, brain, gender identity, and sexual identity
97
Prevalence estimates with transgender people and issues with them
Arcelus et al. (2016) looked at binary trans only * 4.6 in 100,000 individuals. 6.8 for trans females (assigned male at birth). 2.6 for trans males (assigned females at birth). * Though, argued it was an underestimation: Argued an underestimation. This data is based on papers from clinical data. Only based on numbers of people going to clinics. Found that trans women were older, trans men were younger. One reason might be because easier to be a masculine female, than feminine male. Can live well enough just being masculine female. Starting to see flip in this as more trans males than females. data out of date as non-binary not recorded. Persecution (gender/sexuality) in some countries reduce reports. Persecution reduces participation in research
98
Why might there be an increase in reported prevalence on transgender people over the last 50 years?
* Increased acceptance, less discrimination * Better healthcare now. More compassionate process * Though, cultural differences. In Iran, being gay is illegal. Being trans is okay. * Increased education * More diversity in labelling? E.g., no transition desired, but labelling of different gender identity?
99
Diagnosis of gender identity
* Categories gone from sexual deviations to gender dysphoria over the years. Became less stigmatising, and more in line with it being identity and not sexual. * Issue as ICD-10 and DSM-5 both mention distress. Not everybody has significant stress. But some people say in loads of distress to get the help. Not helpful having the criteria people feel they need to fill because subjective criteria anyway. When someone presented for their gender and is significant distress, it is the issue of: we need to treat depression first because might just be due to that, but also do we need to treat the gender identity discomfort first to alleviate that depression. * Causes a vicious cycle. Diagram in notion. * So change to the ICD-11 (2018) as category name change to sexual mental healthcare. Diagnosis name change of gender incongruence. Removed the idea of needing to experience distress.
100
Why have a diagnosis for transgender people? What are the benefits of a diagnosis?
Destigmatise vs access to healthcare. Want to destigmatise something but if completely rid it from diagnostic criteria, then affecting access to healthcare because no longer a health issue Benefits: * Access to healthcare/allows for healthcare costs/ allows for healthcare insurance * Can be validating for some for how they're feeling. Lots of older people like the label and from different era where needed validation of why you are feeling like this * Enables better communication between providers and patients regarding symptoms, prognoses and treatments * Ensures that research can be conducted in homogeneous groups of patients * It allows for epidemiological studies as a basis for research and services planning * It allows for treatment of co-morbid problems
101
Social construction of gender theory
Fallacy of gender dichotomy * Or cultures forces us into binary boxes; allocated on external genitalia * Upbringing can influence gender expression but not gender --> may have gender identity and culture makes us express it in way which might not fit * Trans people in other cultures: Third gender; India Bangladesh, Pakistan (Nanda, 1990). Two-spirit people; indigeneous North Americans (Epple, 1998); Bugis of Sulawesi (Indonesia) have 5 gender categories (Graham, 2004). Because of those places accepting it, don't get co-morbid mental health problems. Always been gender non-conforming people. Cultlures have evolved and defined and there is a social construction putting them into boxes. Also culture and gender stereotypes - e.g., pink and blue colour - see commonly at gender reveal parties
102
Biological aetigoloy of gender identity
* Brains/Genes/Hormones * Area growing and decent amount of research but just not conclusive * During pregnancy: Foetus develops genitals as a result of presence or absence of androgen testosterone. Sexual differentiation of the brain develops later. * Prenatal exposure to sex hormones has led to atypical sexual differentiation of the brain. See at birth affected brain development but don't see this until puberty. Shown in animals if boost testosterone, doesn't change genitals as set and developed, but when animals hit puberty, their beahviours are different. * White matter diagram in notion. * 2D:4D receptors. Higher ratio associated with traits like agrgessions and physical markers like penis size, and cancer (hormone-related). People who are trans males have been more exposed to testosterone in womb because ratio longer.
103
Problems for the medical model of gender identity
* Inconclusive evidence * Not always replicable * More evidence to trans males than trans females (T is powerful) * Risk only trans people who have such biological markers would be accepted thus a means to exclude others * Does not fit non-binary experiences * But - many rely on biology
104
Co-morbidities with transgender people
Transgender people have increased prevalence of: * Self-harm * Suicide * Depression * Anxiety * Interpersonal problems * Susbtance abuse * Eating disorder symptomology Most often predicted by: bullying, transphobia, lack of social support
105
Mental health and transitioning
* Pre-transition: Significantly higher rates of mortality, suicide, suicidal behaviour, and psychiatric morbidity than matched control (Dhejne et al., 2011) * Poor mental health pre-treatment may be caused by waiting times and not pre-existing co-occurring mental health issues (Aldridge et al., 2022) * Post-treatment: Most patients reported improved psychosocial outcomes, ranging between 87% for trans women and 97% for trans men (Green & Fleming, 1990) * Anxiety and depression rates lower if on hormones (Bouman et al., 2017; Witcomb et al., 2018; Aldridge et al., 2020) * Body image better if on hormones (Jones et al., 2017): alleviates dysphoria, hromones help with appearance and "passing" = less discrimination
106
Stigma: The Minority Stress Theory (Meyer, 2003)
Is the problem situated in the individual OR in the society that they are situated in? Applied to trans population because about the stress people feel as a minority. Not experienced by a non-stigmatised situation. Stressors are: * Unique - not experienced by stigmatised populations * Chronic - related to social and cultural structures * Socially based - social pressures, institutions and structures
107
Bullying and gender identity (Stonewall, 2017)
First time they separated LGB students from T students * Transgender students are bullied more than LGB students: 2 out of 3 trans students are bullied. 2 out of 5 students have attempted suicide. 4 out of 5 trans students have self-harmed. * Impacts on day to day day fucntioning and quality of life: lack of feeling safe, lack of social inclusion (mental health suffers) and more on slide Witcomb et al. (2019) * 86.5% reported having experienced bullying, predominantly in school * More prevalent in trans males and in “out” individuals * Individuals who reported having experienced bullying showed greater anxiety symptomology and also self-reported effects on anxiety, depression, and self-esteem * Trans males also reported greater effect on family relationships and social life
108
What is psychosis?
Psychosis is an umbrella term and diagnostic label given to individuals who have experiences that are considered to be outside the ‘norm’ of the individual’s culture. Those with this diagnosis typically: * hear things like voices, * see things others cannot, * hold strong beliefs others dont share e.g., conspiracies against them, * difficulties putting thoughts together coherently, * struggles of concentrating which might refer to thoughts disorder.
109
Types of Psychosis
Psychosis is a set of symptoms, rather than a condition in itself. Diagnoses that an individual with psychotic symptoms may receive include: * SZ - mixture of positive symptoms (presence of something wouldn't expect) and negative symptoms (absence of something would expect e.g., lack of motivaiton) * Bipolar - mood disorder where individual switches from extreme highs (mania) to extreme lows (depression) * Schizoaffective disorder - A mixture of bipolar disorder (depression and/or mania) and schizophrenia (psychotic symptoms) * Drug induced psychosis - Psychotic experiences in the context of using or withdrawing from drugs/alcohol. Often once out the system, psychotic experiences will stop * Psychotic depression - severe depression with psychotic symptoms * Pueperal psychosis - psychosis following childbirth. Often occurs within first hours to first few days after birth. Considered emergency, and mothers hospitalised early on when have this Bipolar prior to pregnancy, 50% likely to have this. * Delusional disorder - holding a firm belief that is not ture
110
Prevalence of psychosis; course and outcomce; mental healthcare
SZ estimated at between 0.2 and 1%. In the UK, 1 in ever 100 people will be given a diagnosis. Tends to be diagnosed in early adulthood (typically between ages 15-35) - Many NHS services nationally will have early intervention and psychosis teams who work with younger clients of 14 upwards as usually prime time of getting it. Affects men and women equally. For every 5 people given a diagnosis of schizophrenia: 1 will get better within 5 years of their first obvious ‘symptoms'; 3 will get better, but will have times when they get worse again - relapse; 1 will have troublesome symptoms for long periods of time. Many people who receive a diagnosis of schizophrenia do not have to go into hospital, and can live meaningful and productive lives Individuals who receive a diagnosis of psychosis are typically seen in secondary mental health services in teams such as community mental health teams and acute psychiatric wards. Assertive outreach teams are for individuals given term of ‘revolving door patients’ who are in an out of hospital. All of these teams work together now and called locality health team, but are still some areas where separated.
111
Issue with diagnoses for psychosis
* Not scientifically valid or reliable, although are presented as objective fact - don't have genetic testing, or blood test, or brain scans. Has to be based on subjective point of view, based on set of criteria. * Do not predict prognosis or treatment response * Are not determined on the basis of objective tests, instead relying on subjective accounts * Decontextualise people's experiences and contexts
112
Continuum Model
* Much research shows that non-clinical populations report having had ‘unusual’ experiences. Such experiences have reported in: Pregnant and postpartum women; Mental health professionals; Primary care patients; Students * This has led to the idea of a Continuum Model of Psychosis, i.e., that there is not a clear divide between those that ‘have’ psychosis and those that don’t, but rather we are all on a continuum * Distress appears to be the key difference between those who seek help and receive a diagnosis of psychosis and those that don’t
113
Usual 'unusual' beliefs - suicide
Questioning unusual by whose standards * Over 5 million people in the UK believe that the moon landings were faked (The Commentator) * 1 in 10 people in the UK has reported seeing a UFO (Huffington Post) * Around 11 million people in the UK have reported experiencing a ‘ghostly encounter’ * Over 57,000 people in England and Wales believe in witchcraft (2011 Census) Suicide * It is estimated that between 5-15% of individuals who receive a diagnosis of SZ will commit suicide * Suicide in such individuals is often done using violent methods * Lopez-Morinigo et al. (2014) - individuals with ‘SZ spectrum disorders’ were significantly more likely to end their lives at a younger age, were more frequently of Black ethnicity and had higher levels of social deprivation than other diagnoses
114
Biological causes of psychosis
* 1 in 100 chance for individual with no relatives with SZ; 1 in 10 for 1 parent with; 1 in 8 for 1 non-identical twin with; 1 in 2 for 1 identical twin. Genetics important but not copmletely causal. There may be relevant non-specific hereditary factors such as temperamental sensitivity and now known genes interact with the environment * Biochemistry: DA hypothesis of overproduction of DA thought still no definitive asnwer. Based on obserations that some medications affect dopamine and can help reduce psychotic experiences and drugs such as amphetamines, which increases dopamine production, can produce psychotic experiences. Though, research still inconclusive. Knowledge of the biochemistry of psychotic experiences is very limited. It may be that the experience leads to biochemical changes or that a third factor (i.e., medication) is responsible for the changes.
115
Critique of biological explanations for psychosis
* Need to remember that psychological changes are equally accompanied by brain changes, and equally our brains are affected by our social experience. Anatomical structures in children can be reduced by sexual or emotional abuse * Bentall (2004) notes there is no test for “schizophrenia”. Blockage of the dopamine system from medication occurs in hours, any benefit takes weeks * Consequently there is a need to realise the bi-directional influence between brain/chemicals and the environment * Unlike with a physical health condition (e.g., cancer, diabetes), there is no brain scan or blood test available to identify someone as having SZ * The diagnosis of SZ is based on an individual making a subjective decision about whether someone sat in front of them for a short period of time meets a range of non-scientifically valid or reliable criteria
116
Social explanations of psychosis: Life events and trauma
* wealth of research showing a link between trauma, particularly in childhood, and adverse life events (e.g. Barrigon et al, 2015; Duhig et al, 2015; Trotta et al, 2015; Read et al., 2012). Read et al. (2012) suggests the evidence so strong that a cause should be suggested rather than a corrleaiton * A review found that between half and three-quarters of psychiatric inpatients had been either physically or sexually abused as children (Read et al, 2008) * Varese et al. (2012) found in their meta-analysis review that greater experience of adversity led to increased rates of psychosis * John Read did brain scans. Previous scan studies show those with psychosis has different brain, but Read found it was identical to those with trauma. Suggests not talking about biological diagnosis but the impact of traumatic childhood experiences. Those experiences lead to change in brain which creates symptoms. Trauma that causes this, not that born with this brain
117
Social explanations of psychosis: Family relaitonships; social deprivation; racism
Family relaitonships: two types of attitudes from family members have been found to lead to poorer outcomes: being critical or actively hostile, and being 'emotionally over-involved'. Social deprivation: link between poverty and psychosis (Kirkbride et al., 2012; Read & Dillion, 2013). People living in deprived inner-city areas are more likely to receive a diagnosis than those in more affluent suburban areas. This link is really important to bear in mind given financial and political climate - 1 in 5 people in UK is thought to now live below official poverty line (Oxfam) Racism: People of Afro Caribbean origin living in the UK are three times more likely to be given a diagnosis of SZ than white people. Potentially due to: social stress nad lack of social support, discrimination (Real or perceived), victimisation and powerlessness
118
Cognitive factors of psychosis: deficits
* Some people with a diagnosis of schizophrenia have difficulties with various aspects of attention, working memory, and executive functioning. E.g., difficult to concentrate cause hearing voices. * Some people with psychotic experiences have problems with social understanding or ‘Theory of Mind’. * Some people who experience auditory hallucinations have difficulty distinguishing their inner speech or thoughts from speech from an external source. Pseudo hallucinations: individuals who report hearing voices but where those voices are attributed to something more internal. E.g., hearing voice of abuser but know it is memory. Diagnosed those more with BPD. People with psychosis will often hear something and attribute them externally. Hear it like someone in the room. * Information processing deficits - People experiencing psychosis have much more cog arousal in a normal day - more likely to be pushed over the info processing threshold (too stressed to remember/process anything). Brain is overloaded, too much stress and information that the brain is trying to deal with and so brain outputs a particular sensation as a voice
119
Cognitive factors of psychosis: biases
* Maher suggests that individuals have ‘anomalous experiences’ which they attempt to explain through normal cognitive processes * People who have delusional beliefs tend to ‘jump to conclusions’ * There is evidence of a ‘confirmatory bias’ in people with psychosis. Look for evidence that confirms their thoughts. If think someone came into the house, will see mug and think they didn’t move that so someone else did. Won’t find things to disconfirm it such as the milk is out so I must have had a cup of tea earlier * Bentall found that some delusions are associated with a ‘self-serving bias’ * People who hallucinate tend to be more suggestible
120
Stress-vulnerability model of psychosis
* Stress-vulnerability model was proposed by Zubin and Spring (1977) * It is suggested that people are believed to be more or less vulnerable as result of biological factors and psychological factors (e.g., temperamental sensitivity) * Sensitivity to particular stresses may also be a result of events that have happened previously in a person’s life * The S-V model is about the Interaction between: - Vulnerability (Long-term/distant) - Stress (Short-term/Recent) - Coping: Personal Factors (e.g., beliefs about experience). Environmental factors (e.g., family, housing) * Bit like weighing scales. Mental health more impacted because ability to cope no longer exceeds to stressors that are present.
121
Stigma around psychosis
Psychosis often linked in the media to dangerousness however research shows that those who receive a diagnosis of psychosis are more liekly to be at risk of harm from others than they are to others
122
Making sense of psychosis
Formulation is the process of collaborative meaning making and is one of the key compentencies for a clinical psychologist. * People's experiences influenced by may factors (e.g., culture, past expereinces) and it can affect a person's distress. But all are unique and hence individual formulation looks different * Formulation looks at assumption that at some point, the person's distress will make sense and that's very powerful and validating to the individual * All psychological formulations: summarise a client's main problems, show how they relate, and lead to intervention plans which are open to revisions and reformulations
123
Psychosis: people's relationship with experiences
* Sometimes people don’t want the voices gone because don’t want to be lonely and it is companionship. Won’t want medication because don’t want the voices to go away. Formulation can help to explore the relationship they have with their experiences. Some might think the voice is God and feel very special because of it. * Cross-cultural studies as Luhrmann et al. (2015) interviewed voice hearers in USA, India and Ghana. Voice hearers in USA were more likely to: believe their voices were caused by genes and described them in diagnositc terms, view their voices as an assault/intrusions into private life; see their voices as being out of their control; see their voices as non-human. Voice hearers in India and Ghana were more likely to: report they had a relationship with voices, feel less troubled by the voices, view the voices as being people, describe their experiences in non-diagnostic terms, view their voices as being spiritual in nature. This study highlights the importance of meaning making in an individual’s levels of distress and they way they cope.
124
Ensuring basic needs are met before therapy for psychosis
Thinking about how to use the formulation to help the person e.g., do they want to reduce stressors in life to cope better? Do they want to voices to stay or go? Because of the level of stigma and distress associated, most won’t have these basic needs. Won’t feel life where they live because believe people out to get you, and if live in place of crime rate, it will maintain that behaviour. - Does the individual have somewhere safe to live? - Have they got food? - Have they got a job? - Are they facing discrimination? - Are they ostracised in their community?
125
Psychological therapy of psychosis
Psychological therapy is based on a psychological framework of understanding (a formulation) and aims to help people work out of the nature of their own difficulties and what is likely to help. Psychological therapy is based on a collaborative and respectful working alliance between professionals and service users. * Psycho-education helps to understand how trauma impacts the brain * Self-monitoring of warning signs and relapse prevention plans. * Adjusting lifestyle patterns
126
CBTp
Nice Guidance (2009) states that: CBT should be delivered on a one-to-one basis over at least 16 planned sessions and: * The aim of CBTp is to: reduce the distress and functional deficits associated with psychosis, rather than to necessarily get rid of the unusual experiences themselves. (Not about getting rid of the voices but to find ways to cope better with those stressors such as trying to stop them from going to alcohol); focus on appraisals of experiences; may also focus on other difficulties e.g., low mood or worry * **look at Garety et al. (2011) and his cognitive model of positive symptoms of psychosis ** * CBTp looks at: whats up (details of their experience); why me (risk factors and trauma); why now (recent triggers); why still (factors maintaining it); what helps (protective factors. Important as good place to start and resoucrces the individual already has). * However, difficult to engage and build up trust so can take a while. Need to make allowances for memory and attention problems.
127
Family Interventions for Psychosis
* NICE guidance (2009) states family intervention should: include the person with psychosis or SZ if practical, be carried out for between 3 months and 1 year, include 10 planned session minimum, take account of the whole family's preference or multi-family group intervention * NICE guidelines recommend that family interventions should be offered to all families of individuals who receive a diagnosis of psychosis or schizophrenia. * Behavioural family therapy (BFT) was developed by Professor Ian Falloon and colleagues in the early 1980’s.Skills-based approach of about 10-14 seassions focusing on communication and promoting positive communication and problem soliving skills. Family can see early signs of relapse and have open, honest and healthy conversations.
128
Various therapies for psychosis
* Trauma focused therapy - focuses on the psychological effects of trauma. Often won't be if in height of the psychotic episode. More for someone further down the line of therapy * Psychodynamic therapy - Focuses on our relationships and how things that have happened in our lives continue to affect us . More for those further down the route * Narrative and systematic therapies. Aims to help individuals fully describe their rich stories and to overcome the effects of narrow and negative stories that are told about them * Voice dialoguing. - A therapist (called a ‘facilitator’) asks questions of an individual’s different ‘voices’ in order to help the person explore, and if helpful to change, their relationship to the voices they hear. Individual invites voices to session and therapist will talk to those voices in turn to try to understand what the different parts are there for and the functions they play in what they are doing for the individual. Slightly newer kind called avatar therapy where individual creates avatar on screen of voice. Put in room with computer and avatar on screen, encouraged to talk to that avatar. Therapist plays the voice for the avatar * Open dialogue. Theoretical underpinning emphasises the importance of social networks and draws upon the notion that ideas and meaning do not arise within individuals’ heads, but emerge in dialogue between people. Born from places like Netherlands and Sweden. Meeting with client with people such as friends, family, employers, mental health team. Opening up dialogue and conversations about what to do to support individual. Medication can be used but rarely used and not used first. Whereas, medication is first-line treatment in the UK. * Acceptance and Commitment Therapy (ACT). Focuses on being present and living life in line with values. Also known as third wave of CBT - more of an emphasis on behaviour. Thoughts and feelings difficult to control but can manage behaviour and response to those thoughts and feelings more * Compassion Focused Therapy (CFT). Focuses on being kinder and compassionate to ourselves, through developing our ability to self-soothe
129
Biolgoical interventions for psychosis
The main drugs prescribed are called antipsychotics. They fall into one of 2 categories: * Typical antipsychotics – the older drugs (e.g. chlorpromazine, haloperidol, flupenthixol) * Atypical antipsychotics – the newer drugs (e.g. clozapine, risperidone, olanzapine). Most of the medications appear to affect dopamine Some psychiatrists are now suggesting adopting a ‘drug-centred’ rather than a ‘disease-centred’ approach. Because don’t have scientific test for SZ, can’t say drug helps it, but can say drug increases appetite and stabilises mood and asking if any of those sounds like it will help you. About a more honest conversation with the individual. Big issues around side effects - physical health and psychological effects. Particularly antipsychotic medication. Can be quite severe. Clozapine can lead to rapid weight gain, much more associated with diabetes and heart disease, lactation in men, erectile dysfunction, cardiac issues.
130
Social interventions of psychosis
* Recovery colleges. - Model also used in other trusts. Peer-led college. Led by people who have often had own mental health experiences and provides a more inclusive and supportive space. * Employment schemes. Getting them in and keeping them in, retention and helping employers understand how to keep their colleagues * Anti-stigma campaigns e.g., Campaign to Abolish Schizophrenia
131
Interventions for psychosis outside of services
Support from family and friends * The Mental Health Foundation’s Strategies for Living project (2000) asked people with mental health problems what helps them the most * Findings clearly showed that it is generally not ‘treatment’ that helps people most, but more everyday things * Most important sources of support identified were relationships with family, friends, and other service users Service User Movements and recovery principles that recovery is possible and unique.Having these psychotic symptoms does not have to stop individuals living a fulfilling life
132
What is IAPT? | Improving Access to Psychological Therapies
Inititiative to try to allow more people over the age of 18 to get professional psychological help. Services which provide evidence-based therapies to people with anxiety disorders and depression. For adults aged 18 and over, who are experiencing milod to moderate psychological difficulties. * Evidence based; community settings; choice of venues' quick access and treatment as people can selfrefer; psychoeducation; guided self help; use of technology such as phone and internet * Involves talking therapies that can be one to one and in groups, plus practical execrsises and tasks both in and outside the scheduled sessions * Therapies widely use CBT for depression, anxiety, PTSD, and social anxiety disorder
133
Stepped care model
IAPT follows stepped care approach Stepped care provides a model for the provision of services; it supports patients, carers and practitioners in identifying and accessing the most effective interventions Those interventions would depend on severity of problems. Trying to find least restrictive and costly interventions that would help people with their psychological difficulties. About tailoring best type of support to needs of client and knowledge that severity and symptoms can vary so the level of training is accordingly needed
134
Effectiveness of IAPT and stepped care model
* Nearly 1.2 million people were able to access services in 2021/22; * 67% who have a course of treatment (two or more sessions) show reliable and substantial reductions in their anxiety/depression; * 51% improve so much they are classified as recovered
135
CBT and its generic framework
* CBT is a model that focuses on the interactions between cognitives, affect, behaviours, and physiological responses (e.g., lack of appetite, no sleep) * Kennerley et al. (2017) do a framwork. Tells us our experiences effects our beliefs and assumptions which iimpact our thoughts. Critical indicents also impact our cognition. These cognitions have itneractions with our physiology, affect and behaviour
136
7 principles of CBT
1. **Cognitive** principle - it is the beliefs about events and situations and not the events and situations themselves that are important (5 people may interpret the same event differently) 2. **Behavioural** principle - what we do has a strong influence on what we think and how we feel. Relationship is reciprocal. 3. **Continuum** principle - our experiences are all on a continuum and mental health difficulties are at the extreme ends of the continuum (shows anyone can have a psychological difficulty because all on a spectrum) 4. **Here-and-now** principle - CBT focuses on currrent experiences and problems instead of past. Doesn't mean disregarded as what's in past might be help but focus on here and now 5. **Interacting systems ** principle - problems can be viewed as interactions between thoughts, feelings, body changes and behaviour based in our environments 6. **Empirical** principle - CBT theory and the applied therapy benefits from on-going evaluation. Therapy is evidence-based and ongoing evluation on whether it's improving for the patient or not 7. **Interpersonal** principle - CBT is a working alliance between patient and therapist. Not an element that is sufficient for the progress but is one of the factors that can contribute to the positive outcome.
137
CBT: three levels of cognition | Kennerley et al. (2017)
1. Automatic thoughts/ negative automatic thoughts 2. Underlying assumptions 3. Core beliefs * 1->3 gets more general, less accesible and harder to change * AT = i'm being boring, i don't know what to say * UA = if people get to know me, then they will find out how useless i am and reject me * CB = i am unloavble, i am useless
138
Automatic thoughts/ negative automatic thoughts
**Our inner dialogue *** These thoughts and images influence our affect. * Common features of NATs include: happen without effort, can easily become conscious, can become habitual so we do not notice them without paying attention to them, they can be mental images as well as thoughts * NATs first described by Beck * NATs are negatively felt appraisals or interpretations that we take from what happens around us. Can be experienced by anyone * Often more prevalent when under pressure; stressed or overwhelmed. Or when a significant event has occurred. * Examples: this is boring, i wish i was paying more attention, did i feed the cat, what's for dinner tonight
139
Core beliefs
**Core beliefs affect the underlying assumptions which can determine our automatic thoughts** * Person’s fundamental beliefs about themselves, other people and the world; Common features: * They are usually learned early in life as a result of childhood experiences. Although they can develop and change later in life for example in response to adult trauma but majority or core beliefs are something that develop in our childhood * They are usually not immediately accessible in our consciousness. Usually somewhere below our consciousness and requires a lot of work to bring them out Examples: Beliefs about selves (I will never be good enough, I am a failure), the world or future (The world is a dangerous place, everything is out of control, i'm never safe), or other people (no relationship lasts, no one understands me, other people are untrustworthy, nobody accepts me for who I am)
140
Underlying assumptions
**UAs bridge the gap between core beliefs and automatic thoughts** * Often develop in response to the core beliefs * They are usually conditional statements including 'if...then/shold/must/otherwise' * They can become 'rules for living' developed from experience and the presence of the core beliefs * They can be a persons strategy for living with the core belief and if this is negative then they can become dysfunctional * Dysfunctional assumptions are rigid; over-generalised; inflexible and illogical when reviewed in a objective way
141
Cognitive distortions
Unhelpful thinking patterns which may come as a result of difficult life experiences or be learnt. They may sound "rational" on the surface, but are usually incorrect and inaccurate when examined more closely Common cognitive distortions are: * All or nothing thinking * Overgeneralisation - seeing one even as a pattern of never-ending defeat. See the word 'always' and 'never' here * Negative mental filter - dwelling exclusively on the negative elements of our experience * Catastrophising - exaggerating meaning and consequences of that event * Should statements * Self worth
142
Process of CBT
1. CBT **assessment** identifies the cognitions that people have and how their responses to those cognitions can maintain their problem experiences 2. CBT **formulation** is the development of a shared understanding between therapist and patient of the problems being discussed 3. CBT **intervention** is the method of supporting a person to learn new ways of thinking or behaving to reduce problems 4. CBT **evaluation** occurs throughout the intervention and is a way of monitoring the progress on individualised treatment goals
143
Key Strategies and Tools
* Agenda setting * Goal setting * Identifying activating events * NATs * Maintenance cycles * Core beliefs * Socratic questions (guided discovery) * Cognitive challenging * Cognitive restructuring * Psychoeducation * Homework * Thought diaries * Mood monitoring * Fact vs Opinion * Behavioural experiments
144
Socratic Method
* Socratic questioning allows the therapist and the client to explore what the clients already know and what they have not considered yet, or have forgotten * During the Socratic questioning, clients are encouraged to discover alternative views and solutions for themselves * Can be helpful in clarifying the meaning of problems and in order to re-evaluate previous conclusions * Examples in assessment and formulation: what did it mean to you when you thought/did that? What does through your mind when you feel like that? * Examples in challenging unhelpful cognitions: how helpful, or unhelpful, is it to hold this particular belief? What is the downside of seeing things this way?
145
Cognitive and physical techniques of CBT
Cognitive techniques * Identifying cognitions - diary keeping. Situation - feelings (+ level of discomfort) - thoughts * Enhancing recall through imagery and role play * Clarifying global statements (e.g., "In what way useless?") Physical techniques * Relaxation - to help with physical tension (anxiety, depression) * Controlled breathing (hyperventilating as one of the benign symptoms of panic attacks) * Physical exercise. NICE recommends that all patients with mild depression should be advised on the benefits of structured exercise programme (NICE, 2004a)
146
Definition of formulation in CBT
A provisional map of a person’s presenting problems that describes the territory of the problems and explains the processes that caused and maintain the problems *Bieling and Kuyken (2003)*
147
Properties and elements of case formulation in CBT
Properties of case formulation in CBT * Describes and explains presenting problems in terms that can be operationalised (what cognitions, what affects, what behaviours) * Is reliable and valid * Provides guidance for intervention * Is an active and ongoing process, responsive to new date Elements of case formulation in CBT * Description of presenting problems (in clear, specific and measurable terms) * Developmental history * Causal factors * Maintaining factors * Guides or intervention
148
What is CBTp?
Turner et al. (2014) said it aims to promote awareness of the links between thoughts, behaviours, and feelings to help implement changes in symptoms and functioning It is all about the appraisal of that experience. * The goal is not necessarily to stop people from having psychosis, becuase this is not realistic. The goal is to stop the condition providing dysfunction or distress.
149
What is CBTp for?
* Number of ways in which CBT has been used in the field of psychosis * Reduciton in symptoms severity: delusions, hallucinations, negative symptoms * Preventing relapse: stopping the person becoming unwell again
150
Hierarchy of Evidence
Need systematic reviews because often smaller studies have low power. So when pull studies together, can see strong effect. From background information -> case-controlled studies -> cohort studies -> RCTs -> critically appraised individual articles -> critically appraised topics -> systematic reviews
151
Efficacy vs effectiveness (Porzsolt et al., 2015)
* Effectiveness of an intervention - assessed by 'observation of real-world healthcare'. Whether it works in real life * Efficacy of an intervention - obtained from experimental studies. Provides much better evidence - RCTs.
152
Weaknesses of effectiveness trials
* Because often don't have control gorup, may have situations where people would have improved anyway * Problem with RCTs as might get randomised into therapy or no therapy. Might do badly in that treatmment due to resentment from that immoralisation. * When compare two therapies together, often little difference
153
CBTp for preventing relapse (Bighello et al., 2021)
Relapse is associated with: - Hospital admission (high cost) - Unemployment - If in hospital, might lose job because not working - Risk to relationships - Risk of suicide - People find having a severe and enduring mental illness a hard thing Bighelli et al. (2021) ⇒ relapse at 3 different time points (6 months, 12 months, more than 12 months). CBT was effective at 6 months. Significant effect for CBT reducing relapse after 12 months. CBT approaches demonstrated some evidence for keeping people out of hospital for period of about a year. Also family interventions, and relapse prevention programmes. Yet, therapy is not medicine. Therapy done by and with people, and very hard to do that in a very consistent way.
154
Effective vs non-effective CBTp for relapse prevention (Dunn et al., 2012) - factor analysis of therapy scale
Dunn et al. (2012) wanted to find out how CBT worked. Analysis of recordings from 1019 sessions with 102 patients using a validated therapy scale Said can divide therapy sessions by 2 types. Degree to which first and second factor happened in therapy First factor: partial thearpy => - Engagement and assessment techniques - Collaborative assessment of psychotic experiences and delusional beliefs Second factor: full therapy => - Relapse prevention interventions - Enhancing self-regulation - Development of a personal model of relapse - Work to re-interpret meaning of the experience of psychosis - Schema work Found the people who received the full therapy were the ones less likely to have a relapse. Partial therapy had some indication might relapse sooner. Full therapy had about 5 1/2 months of being well. Full treatment leads to nearly six months in remission, partial treatment may have a negative effect
155
CBTP for relapse prevention
- There is evidence that CBTP reduces relapse rate/increases time before relapse - BUT, it is important that patients receive FULL therapy as indicated by Dun et al (2012) - AND this is not easy … Jolley et al found that only 37/58 course attendees were able to achieve ‘objective competence’ in the delivery of CBTP - Really hard to do - Important when reading trials to check for fidelity, degree to which the evidence of the researcher sticks to the script because that often doesn’t happen
156
CBTp for reducing symptom severity
Find CBT reliably associated in reductions of experiences. and hallucinations but less on delusions. - Most therapy trials don’t really seek to change diagnostic status, rather they aim to reduce distress and unhelpful/risky behaviours - Outcomes are often measured using the PSYRATS (interview assessments of difficulties associated with delusions and hallucinations) and/or the Green Paranoid Thoughts Scale. Other assessments such as the Positive and Negative Symptom Scales (PANSS) are also used
157
CBT for command hallucinations A good example of CBT not being quasi-neuroleptic (Birchwood & Trower, 2006)
Drive now to say we know the therapies work, and know what the ingredients of good therapy are but even if know what those ingredients are, we don’t know the mechanisms and changes. - Only really have an idea for it for this particular therapy - Command hallucinations are instructions to do - People have to come to conclusion about what’s going on and with their beliefs about the voice itself, and will have a relationship with that voice. Humans do not like uncertainty. - People demand explanations. Issues are when people have a very damaging appraisal of it, e.g., my thoughts are the devil, FBI etc. - This model says people hear the voice, develop a power and authority of the voice, and leads to affective and behavioural consequences. Consequences such as carrying knives. - According to this model, trying to reduce the person’s belief in the power of the voice
158
Cognitive therapy for command hallucinations (Trower et al., 2004; Birchwood et al., 2014)
Found if you reduce people’s belief in the voice power differential, people don’t do what the voice says anymore. Going from thinking the voice is the devil, to not knowing who it is and realising it isn’t powerful so don’t need to do what it says, means no reason for appeasement or harmful compliance. Mechanism definitely that difference to power
159
Garety et al. (2001)
Cognitive model for positive symptoms of psychosis. You have a genetic vulnerability which is triggered. This causes emotional changes and cognitive dysfunction which makes the brain appraise experiences as something external. These are the positive symptoms. These positive symptoms are maintained by things such as: reasoning and attributional bias, dysfunctional schemas, emotional processes and appraisal of psychosis. Highlights the role of appraisal and making sense.