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History of diagnostic concepts and systems, anxiety conditions, mood conditions.
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What did Karl Ludwig Kahlbaum do?
Tried to develop classification system that grouped mental diseases according to their course and outcome
Stressed importance of parental upbringing to prevent ‘Juvinile Madness’
What did Emil Kraepelin do?
Wrote the Compendium of Psychiatry - used detailed case studies & methods such as clinical observation, psychological tests and psychopharmacology.
First described schizophrenia, which he called ‘dementia praecox’, and differentiated it from manic-depression and paranoia
What did Helen Boyle do?
First female president of the Royal College of Psychiatrists
Focused on helping women living in poverty by offering free and low-cost mental health care at the Lady Chichester Hospital in Brighton
Set up to reduce amount of women ending up in asylums
Lady Chichester was the first faculty to offer early intervention systems
What did Eugen Bleuler do?
Published Lehrbuch der Psychiatrie, which listed the fundamental symptoms of dementia praecox as
- Ambivalence
- Inappropriate affect
- Loosening of associations
- Autism
And the accessory symptoms as
- Hallucinations
- Delusions
What did Kurt Schneider do?
Distinguished between ‘form’ and ‘content’ of disorders
“Diagnosis looks for the ‘how’ (form) not the ‘what?’ (content)
What did Karl Jaspers do?
Questioned popular understanding of mental illness and diagnostic criteria
Controversially stated abnormal experiences can occur through normal cognitive processes
Published General Psychopathology, which influences many current diagnostic criterea
What is the evolution of the concept of bipolar disorder?
Kraepelin - Grouped all affective psychoses into a single category of manic-depression
Klaus Leohnard - observed some patients experience both manic and depressive episodes, some only depressive
By 1970s, it had become commonplace to distinguish between unipolar and bipolar disorder
What lead to the development of the DSM?
At the end of WWII, seperate army, navy, airforce and civilian classifications were in use.
The APA formed a task force in 1948 to create new standardised system
DSM published in 1952
What lead to the inclusion of psychiatric illnesses in the ICD?
In 1948, WHO tasked with creating an International List of Causes of Death
When creating ICD-6 in 1951, WHO added nonfatal diseases including psychiatric diagnoses.
In 1960s, APA began revising DSM-I to make it more consistent with ICD-8.
Who suggested the criterion ‘reliability’ and ‘validity’ for evaluating diagnostic systems?
Spitzer and Fliess (1974)
Define reliability
The extent to which diagnosticians can agree about who had what diagnosis
Define validity
The extent to which the diagnostic system is useful for the purposes intended
What was initially described as the ‘satisfactory’ Kappa score?
0.70
What happened during DSM-III field trials?
Kappa values often failed to exceed 0.7
What did Krueger et al. propose as an alternative model of classification?
The Hierarchical Taxonomy of Psychopathology (HiTOP) model
What are some benefits of the HiTOP model?
Removes arbitrary boundaries between psychopathology and normality
Focus on symptoms as opposed to diagnosis
Easier to explain co-morbidity due to hierarchical structure
Higher test-retest reliability than traditional classification systems
Limitations of HiTop model?
Created using simple structure factor analysis approach - does not accurately represent dimensional space of the symptoms of psychopathology
Dimensional ratings do not fix problems inherent to descriptive classification
No clinical evidence found suggesting clinicians using HiTOP have better clinical outcomes than those using DSM.
The DSM-IV included an exclusion for which stressor when diagnosing depression?
Bereavement
How did the DSM-V differ from DSM-IV?
Removed all exclusions for stressors
What is the core symptom of a major depressive episode?
Depressed mood or loss of interest/pleasure (anhedonia)
What are the other symptoms of a major depressive episode?
Weight loss/gain
Insomnia/hypersomnia
Psychomotor agitation or retardation
Fatigue
Feelings of worthlessness or excessive guilt
Difficulty thinking, concentrating or making decisions
Recurrent thoughts of death or suicide ideation
What are the conditions of a major depressive episode according to DSM 5?
5 or more symptoms (including core symptom)
Symptoms present for at least 2-week period
Causing significant impair or distress
Not due to physiological effects of a medical condition
What is major depressive disorder?
Has at least one major depressive episode, and no mania or hypomania before or during.
What is persistent depressive disorder?
At least 2 years of consistent depressed mood, with no more than 2 month gaps
At least two symptoms like those of major depressive disorder
No mania or hypomania before or during
Over one year in children & adolescents
What are three sub-type diagnoses of depression?
Anxious distress
Psychotic features
Seasonal pattern
What is premenstrual dysphoria disorder?
Depression related to menstrual cycle, distinguished from typical premenstrual cycle, new addition to DSM 5.
What is a concern regarding premenstrual dysphoria disorder?
Potential stigmatisation of typical menstrual cycle
What exclusionary factor was removed from the DSM 5?
Grief
Why was grief removed from DSM 5?
Considered fundamentally different from MDD, removed to prevent obstructing treatment.
What % of adults in the UK have been diagnosed with depression?
19%
What condition is highly co-morbid with depression?
Anxiety
In what groups are depression rates highest?
People aged between 18-29, women
Define relapse
Return of difficulties within a short timeframe
Define recurrence
New episode of difficulties
What are the biological factors associated with depression?
Genetic vulnerability
Neurotransmitters
Brain structure and functioning
Overactive Hypothalamic-Pituitary-Adrenal Axis
How do genetics influence depression?
1st degree relative with depression = 2-3x more likely to also develop.
How do neurotransmitter effect depression?
Monoamines including norepinephrine, serotonin, dopamine
Serotonin and norepinephrine synthesis, release or reception may be abnormal
HOWEVER recent review suggests no consistent evidence of serotonin theory of depression
How does brain structure and functioning affect depression?
Pre-frontal cortex - reduced metabolic and brainwave activity, reduces grey matter.
Anterior cingulate - differing activity to non-depressed
Hippocampus - reduced volume, reduced metabolic activity
Amygdala - increased activity
How does overactive HPA axis affect depression?
High levels of CRH and cortisol
Inhibits receptors for monoamine neurotransmitters
Impacts brain structures
What psychological factors are associated with depression?
Behavioural theory
Cognitive theory
Reformulated learned helplessness theory
Cognitive factors involved in depression
Behavioural theory of depression
Stress/negative event → depressive mood → less activity and withdrawal → fewer natural reinforcers → further depressed mood
Cognitive theory of depression
Cognitive triad (negative view of life, world, future)
Early adverse experiences → core beliefs and cognitive vulnerabilities → activation of beliefs due to cognitive biases → depression
Reformulated Learned Helplessness theory of depression
The understanding we form of our experiences can be associated with our mood
Internal vs External, Stable vs Unstable, Global vs Specific
Way of thinking = greater vulnerability to depression
Cognitive factors involved in depression
Cognitive biases (ways of processing)
Cognitive emotion regulation strategies (rumination, distraction…)
Cognitive control on depression
What social factors are associated with depression?
Social factors as triggers for depression → difficulties in interpersonal relationships precede depressive episodes
Social difficulties due to depression → higher likelihood of relationship conflict and social skill difficulties
Component of difficulties → elevated feedback seeking (positive and negative), perception of rejection from others
Biopsychosocial theory of depression

What is the Matched Care Model?
Ensures most effective, least intrusive and least resource intensive treatments are delivered first.
Allows access to more intensive treatments if and when needed
Considers other factors (pt presentation, pt choices and preferences, previous tx)
What are the categories for severity of depression?
Sub-threshold depression → <5 symptoms
Mild depression → 5 symptoms, minor functional impairment
Moderate depression → Symptoms or function impairment between ‘mild’ and ‘severe’
Severe depression → Most symptoms present, considerable impact on functioning
What are the biological interventions for depression?
Antidepressants (MAO inhibitors, Tricyclic antidepressants, SSRIs, SNRIs)
Electroconvulsive therapy
Repetitive Transcranial Magnetic Stimulation
How do monoamine oxidase inhibitors work?
Inhibits monoamine oxidase enzyme which breaks down neurotransmitters such as serotonin and dopamine
How do tricyclic antidepressants work?
Block serotonin and norepinephrine reuptake within the presynaptic terminals
Differ from SNRIs as they are less selective and carry a higher risk of side effects
How do SSRIs work?
Block serotonin reuptake within the presynaptic terminals
How do SSNRIs work?
Block serotonin and norepinephrine reuptake within the presynaptic terminals
How effective are antidepressants?
Relative equivalence in effectiveness between antidepressants
Approx 50-60% experience some improvements
Different side effects for different medications
When antidepressants compared to placebos, medication was found to be no better than placebo except in very severe depression
What is ECT?
Inducing seizures by passing electrical current through the brain
What are the side effects of ECT?
Memory loss, slowed response, difficulty learning new information
Who is ECT reccomended to?
Individuals with severe or treatment-resistant depression
What is RTMS?
Administering magnetic pulses to the brain, targeting the left prefrontal cortex.
Few known side effects and considered safe, however requires more evidence to evaluate.
Currently appears to have short-term efficacy
What are the psychological interventions for depression?
Cognitive behavioural therapy
Behavioural activation
Mindfulness-based Cognitive Therapy
What is Cognitive Behavioural Therapy?
Derived from the work of Beck et al. and formed of 2 main components:
Cognition → Changing negative thoughts and beliefs
Behaviour → Changing actions`
What is behavioural activation?
Based on behaviour theory of depression: therapeutic focus of increasing activity.
Increasing activity levels allows for more positive reinforcement and a reduction in avoidant behaviours.
It also allows us to increase our understanding of our current behaviour by encouraging monitoring of daily activities and how they effect our mood, design personally meaningful goals and acts based on structure not based on mood.
What is the ABC of functional analysis?
A - ANTECEDENTS - What is the situation?
B - BEHAVIOUR - What does the person do?
C - CONSEQUENCE - What happens as a result?
What is mindfulness-based cognitive therapy?
Combines CBT and mindfulness-based stress reduction
Learning to observe as opposed to engage with depressive thoughts and feelings
Considered particularly helpful for recurrent depression
What are the social interventions for depression?
Interpersonal therapy
Behavioural couples therapy
What is interpersonal therapy?
Focuses on 4 general areas:
Grief about loss
Relationship conflict
Change relating to interpersonal roles
Social/communication skills
What is behavioural couples therapy?
Specifically designed intervention to change the nature of interactions between the participants and develop a more supportive relationship with less conflict.
Effectiveness of psychological interventions
Compared to controls, treatment effect appears moderate to large
Compared to antidepressants, treatment effect appears comparable
Compared to each other, treatment effects appear largely comparable
CBT associated with significant reductions in mental health problems
However, quality of evidence is limited
What are the NICE recommended interventions for less severe depression?
Guided self-help
Therapy (inc. CBT, BA, IPT, mindfulness counselling)
Individual/group settings
Group exercise
SSRIs
What are the NICE recommended interventions for more severe depression?
Combination therapy and medication
Individual therapy (CBT, BA, IPT, mindfulness counselling, individual problem-solving)
Medication (SSRIs, SNRIs or others based on clinical history)
Guided self-help
Group exercise
What is the guidance on relapse prevention for depression?
Those with significant risk of relapse should be considered for continuation of support and development of relapse prevention skills.
What are some physiological components of the fight or flight response?
Slowed digestion, pupil dilation, reduced saliva, fast breathing, increased heart-rate, decreased motility of the large intestine, epinephrine production
How does anxiety differ from fear/panic?
Anxiety is an adaptive reaction that primes the individual for the fight/flight response
Anxiety is future-focused
Anxiety centralises on uncontrollability and future threats as opposed to actual danger
At what point does anxiety become a disorder?
When it can be considered ‘maladaptive’ - impaired daily functioning, unmanageable levels of anxiety, unexpected onset of anxiety
What 5 primary types of anxiety disorder does the DSM-5 recognise?
Specific phobia
Social anxiety disorder
Panic disorder
Generalized anxiety disorder
Agoraphobia
What are the symptoms of a phobia?
A fear or anxiety about a specific object or situation, in which the fear or anxiety if out of proportion to the danger posed
The fear and anxiety or avoidance of the phobic object is persistent
Causes clinically significant distress or impairment
What are some sub-types of phobias in the DSM-5 and DSM-5-TR?
Animals
Natural environments
Blood/injection/injury
Situational
Other
What is the lifetime prevalence for phobias?
12%
What is the age of onset for phobias?
Onset varies widely and persists over decades
What are the gender differences in phobias?
More common in women than men, but the gender ratio depends on the type of phobia
What has high co-morbidity with phobias?
Other anxiety disorders and mood and substance use disorders.
What are the psychological causal factors of phobias?
Psychoanalytic theories
Learned behaviour (including vicarious conditioning, individual differences in learning, evolutionary preparedness)
Psychoanalytic theory of phobias
Defence against anxiety that stems from repressed ‘id’ impulses, externalised as a defence mechanism
Vicarious conditioning theory of phobias
Person-to-person observation of someone reacting to their phobia, or observation of a non-fearful person experiencing a fear-provoking event leads to development of phobia
Individual differences in learning theory of phobias
Everyone has their own experiences and risk vs protective factors
Evolutionary preparedness theory of phobias
Not innate but more easily acquired, where the conditioning to the fear-relevant stimuli is more effective
Biological theories of phobias
Temperament
Genetic
Temperament explanation for phobias
Behavioural inhibition (being shy, avoidant) personality type, starts early in childhood, shows motivation to avoid aversive outcomes.
Genetic explanations for phobias
Modest heritability shown in twin studies, phobias more related to individual experiences and differences
What types of exposure therapy are there?
Modelling
Flooding
Systematic desensitisation
Virtual reality exposure therapy (VRET)
Modelling exposure therapy
Based on SLT, imitation based on behaviour helps gain coping skills and self efficacy
Flooding exposure therapy
Emphasises habituation to the phobic stimuli. Single sessions of exposure have been found to be effective in phobic stimulus such as small animals and claustrophobia.
New research on flooding exposure therapy
Knowles and Olatunji (2019) have suggested strengthening inhibitory association as opposed to habituation
Systematic densensitisation exposure therapy
Focus on reducing sympathetic activity via relaxation training before gradual exposure to a fear hierarchy. Based on the premise that anxiety and relaxation cannot co-exist.
Virtual reality exposure therapy
Combination of in vivo and imaginal exposure, Botella et al. (2017) found in a systematic review that the control, flexibility and safety of the individual were advantages however it is not equally effective in all patients
What are the symptoms of social anxiety disorder?
A persistent fear or one or most social or performance situations
The person recognizes that the fear is unreasonable or excessive
The avoidance, anxious anticipation or distress interferes significantly with the person’s daily activities
What is the lifetime prevalence of social anxiety?
12%
What is the age of onset for social anxiety disorder?
Most common in adolescence and early adulthood
Why may adolescence be a common time for social anxiety to develop?
The most rapid phase of human development, changes in cognition, body image and body dissatisfaction, emotional and sexual identity.
What are the rates of co-morbidty in social anxiety?
90%
What other conditions are regularly comorbid with social anxiety?
Specific phobias
Major depressive disorder
Alcohol use disorder
Eating disorders