Cognitive theories of emotional disorder - summary of chapter 4 of Cognition and emotion: from order to disorder

Cognition and emotion: from order to disorder
Power, M. & Dalgleish, T. (2015).
Chapter 4 
Cognitive theories of emotional disorder


Introduction

There are a number of influential cognitive approaches toe motion that have their starting points to be disorders of emotion.

Cognitive approaches to the emotional disorders have typically focused on a specific disorder.
This carving up of the emotional disorders can lead to a false sense of disjointedness between the emotions in comparison to the more over-arching theories.

Seligman’s learned helplessness theory

Learned helplessness

The role of perceived non-contingency plays an important role in the theory of learned helplessness.
The original theory focused on the key features of passivity and helplessness in the face of future events characteristic of depression.

Reformulated learned helplessness

Abramson added Weiner’s attribution theory to the original learned helplessness approach.
Although helplessness continued to be seen to arise from the perception of uncontrollability, the subsequent effects were now seen to depend both on the type and the importance of the event experienced, together with the explanation that the individual produced for the cause of the event.

The explanatory style dimensions focused on three of Weiner’s attributional dimensions

  • Internal-external or locus
    Whether the cause is seen to be due to something about the individual (internal) or due to something about other people or circumstances (external)
  • Stable-unstable
    Whether the cause is due to something that would recur future similar events
  • Global-specific
    Whether the cause influences only one area of the individual’s life or many

The combination of these dimensions led to the proposal that the emotional, motivational and cognitive deficits seen in depression could be accounted for by a particular set of attributions following the occurrence of a negative event.

The crucial type of attribution style that is identified as a vulnerability factor for depression is if the individual makes internal-stable-global attributions for the causes of negative events and external-unstable-specific attributions for positive events.
An internal attribution for a negative event leads to low self-esteem, especially if other individuals are perceived not to be helpless in such a situation (personal helplessness).
The additional stable and global attributions for negative evens add to the chronicity and the generality of the deficits observed in depressed individuals.

It is possible that depressogentic implicit attributional tendencies are not being detected by the routine questionnaire methodology.
The links between style and emotion can be weak correlational ones.

Hopelessness theory

Hopelessness theory is a reformulation of helplessness theory.
The key differences is that hopelessness requires only the occurrence of negative events rather than uncontrollable events.
The main outcome is hopelessness rather than helplessness. This places the emphasis on negativity.

Hopelessness makes some adjustments to the combinations of the attributional dimensions and their consequences.
Low self-esteem is now seen to derive from an internal-stable-goal attributional style.
A combination of stability and globablity is seen to lead to generality and chronicity of depressive deficits.  

Beck’s cognitive therapy

Cognition is not the cause of emotional disorders, but it is part of a stet of interacting mechanisms that include biological, psychological, and social factors.

There are two main components to the theory from which the general therapeutic approach is derived

  • The types of cognitive structures that underlie the emotional disorders
  • The types of cognitive processes that are involved in the onset and maintenance of these disorders.

Beck’s model of depression
Early experience à Formulation of dysfunctional assumptions à Critical incidents à Activation of assumption à Negative automatic thoughts à depression

The type of knowledge representation that cognitive therapy focuses on is schemas.
Schemas are seen to be units in which memories, thinking and perception are organised.
These schemas are in part derived from past experience, but are not passive representations of that experience. Activation of part of the schema leads to activation of the whole schema. Information not represented in the input will be filled in according to operative ‘default’ values.
The patterning of self-schemas and significant-others schemas, which is based on past experience, will provide a starting point from which current relationships and experiences are viewed.

In relation to specific emotional disorders, certain groups of dysfunctional schemas are likely to be characteristic.

  • Depression
    Schemas reflect cognitive triad that focuses on negative views of the self, the world and the future

Between episodes of emotional disorders, Beck proposed that dysfunctional schemas are inactive and lie dormant.
They become activated only when appropriate matching stressors occur.
Part of the reason for this proposed latency of dysfunctional schemas has been to immunise the theory against failure to find elevated levels of dysfunctional attitudes and automatic thoughts during recovery.

But, it seems unlikely that such important concerns for the individual become inactive.
Alternative possibilities are that the dysfunctional schemas remain active but that during recovery the individual is able to inhibit the outcomes of such processing if it is negative, or if the outcomes of processing are positive these are consciously acceptable to the individual.
Another possibility is that the traditional view of schemas is too simplistic to capture the type of high-level representation system necessary within cognition-emotion systems.

The effect of activation of dysfunctional schemas is that they produce negative automatic thoughts which the individual believes.
Unlike healthy individuals, who can normally dismiss such thoughts, depression-prone individuals may seek further evidence in support of such negative thoughts and beliefs.
This evidence-seeking includes the logical distortions of thinking.

  • Magnification
    Negative material related to the self
  • Minimisation
    Positive material related to the self
  • Personalisation
    Taking the blame for anything negative

The outcome of these distorted processes, in combination with other biases such as for memory, is that the depressed individual maintains a negative view of the self and thereby remains depressed.

Two main points to raise about this view of cognitive processes

  • The approach implies that normal thinking is logical and rational
    But whether or not this is true remains unresolved
    The differences between normal and depressive thinking may be less that of logical versus illogical thinking and more that of positively biased versus negatively biased processes
  • It presents a view of self-concept in depression that is monolithic and negative
    One puzzle to which cognitive therapy fails to provide an adequate answer is how the self-concept switches form being negative during an episode of depression to being positive during recovery

Clark’s adaptation of cognitive therapy for panic

The key theme in both Beck’s general approach to anxiety and in Clark’s application of the approach to panic disorder is that the individual is considered to be prone to the detection of threat or danger in both the external and the internal environment.
The catastrophic misinterpretation of the environment maintains the high level of distress experienced in a panic attack. It may also lead the individual to become hypervigilant for particular bodily sensations and likely to avoid situations or activities that produce similar sensations.
Despite the avoidance, the hypervigilance will still lead the individual to detect small physical sensations, which push the individual into a vicious circle.

Williams, Watts, MacLeod and Mathews (1988, 1997)

The network theories of Bower and the schema theory of Beck predicted that a wide range of cognitive biases should be found in emotional disorders.
There is a failure to find such global biases.

Williams proposed an empirically based model in which cognitive biases were specific to specific emotional disorders.
Williams took as theoretical starting point the distinction between

  • Priming
    An automatic stage of processing in which the stimulus may be linked with its representation in long-term memory
  • Elaboration
    Subsequent strategic or resource-demanding processes

In the case of anxiety disorders, Williams propose that automatic priming processes are biased towards the detection of anxiety-relevant stimuli or situations.
Although initial priming or automatic processes are biased towards the detection of threat in anxiety, subsequent elaborative processes are biased away from the processing of threat.

The main cognitive biases evident in depression are resource-demanding elaborative ones that are most apparent in mnemonic tasks.

The strength of the framework presented by Williams et al is that it provided a focus for the dissatisfaction for global cognitive biases.
But, Williams provides a starting point rather than an aetiological theory.

Teasdale and Barnard

The interaction cognitive subsystems (ICS) approach is an exemplar of one of a class of multi-level, multi-system approaches which, can provide accounts of a variety of cognitive skills and processes.
The link between cognition and emotion is not easily pinned down in such models, because the relationship is seen as complex and interactive.

Nine cognitive subsystems in Teasdale and Bernard’s ICS approach

  • Sensory related

    • Acoustic subsystem  
    • Visual subsystem
  • Central subsystems
    • Morphonolexical
    • Propositional
    • Implicational
    • Object
  • Affector subsystems
    • Articulatory
    • Body state
    • Limb subsystems

These subsystems process information partly in parallel and partly sequentially according to the type of task and other requirements acting on the overall system

In relation to emotion, the key subsystems are the propositional and the implicational subsystem.
The units of representation in propositional subsystems do not have truth values in themselves but are merely names about which noting is asserted.
Only when included in larger units do the units become propositional and they are either true or false.
The higher-level semantic representations at the implicational level in ICS are referred to as ‘schematic models’.
Schematic models combine information for a variety of sources.

Four of the key sub-systems involved in the occurrence of emotion in the ICS approach

  • Visual subsystem
  • Implicational subsystem
  • Propositional subsystem
  • Body state subsystem

In the ICS approach, emotion is the result of the combination within the implicational subsystem of outputs form a number of cognitive subsystem.

In ICS, automatic thoughts may be the consequence rather than the cause of depressive schematic model at the implicational level, though in turn these negative thoughts may serve to lock the system in a depression-maintaining loop.

Teasdale and Barnard argue that much of the challenging of negative thoughts and beliefs in standard cognitive theory occurs at the propositional level and may often ignore the higher level implicational meaning. This can make the depression worse.

A focus on the implicational level of meaning would suggest that an important issue for a client might be a need to discover things for himself and that a focus on the therapeutic relationship in relation to this and other issues might be well warranted.

  • Intellectual beliefs
    Meanings at the propositional level
  • Emotional beliefs
    Propositional articulations of schematic models at the implicational level

The information held at the two levels need not be consistent.

The central distinction between the propositional and the implicational levels of meaning may not be as clear-cut in practice as it appears.

Social-cognitive theories

In social-cognitive theories of psychopathology it is argued that vulnerability to emotional disorders cannot solely be located in factors internal to the individual nor in factors that are solely external.
There is a complex interaction between the internal and the external.
There is a type of diathesis-stress model in which an external stressor is problematic for an individual with a relevant vulnerability.

Social-cognitive theories of depression

Social-cognitive theories of depression focus on a number of related proposals

  • The vulnerable individual has a high level of investment in one particular role or goal
  • The individual may pursue this role or goal, with considerable success
  • The occurrence of a severe event which matches the role or goal thematically, and which thereby threatens it, increases the likelihood of depression
  • The influence of social-cognitive factors is seen to be the strongest for first episodes of unipolar depression, but the repeated experience of adversity and depression may lead to a sense of ‘defeat’ in which the individual disinvests in all domains, including those which were previously overinvested
  • Most theories identify a number of other vulnerability or protective factors
    • Whether or not the individual has a close confiding relationship
    • Issues such as self-esteem and self-concept
    • Attributional style
    • Dysfunctional attitudes
    • Coping
    • Emotion regulation strategies

Weak points of social-cognitive theories of depression

  • There has been poor agreement over the measurement of social factors
  • Social-cognitive models often appear to hedge their bets over whether they are models of the onset of disorders, of the maintenance of disorders, of the recovery from disorders, or of relapse of disorders
  • The models are often poor at explaining how vulnerability factors arise in the first place
  • Social-cognitive accounts of depression are well in advance of equivalent accounts of other disorders

Miscellaneous theories of emotional disorders

Emotional processing

Emotional processing is used in reference to how an individual processes stressful events.

The proposal is that it is inevitable that unpleasant events will occur to an individual at one time or another, but the consequences of such events are normally satisfactory processed.
Evidence of normal emotional processing is provided 

  • Emotional disturbance has occurred
  • The disturbance eventually declines in strength
  • There is a return to routine behaviour

In abnormal grief reactions, there is a failure in this normal sequence, which is likely to result from a failure of emotional processing.
A number of indices by which these failures can be identified

  • The presence of direct signs

    • Obsessions
    • Disturbing dreams
    • Unpleasant intrusive thoughts
    • Inappropriate expressions of emotion
    • Behavioural disruptions
    • Pressure of talk
    • Hallucinations
    • Return of the fear after a period of absence
  • Indirect signs
    • Subjective distress
    • Fatigue
    • Insomnia
    • Anorexia
    • Inability to direct constructive thoughts
    • Preoccupations
    • Restlessness
    • Irritability
    • Resistance to distraction

What types of emotion modes are needed to account for the observation that individuals may fail to process stressful events.
We can consider a cognitive conflict model in which the unwanted material is inhibited because it conflicts with core self-beliefs, important goals and plans, or important beliefs about significant others.
The more dramatic or severe the stressful event, the greater the impact on the individual’s beliefs, goals and plans. Denial causes clinical worry.
A cognitive account of limited attentional resources may have to be allocated in order to maintain cognitive and behavioural avoidance.

Summary

  • Several types of theories point to the key role that significant events play in the emotional disorders.
    It is not simply that such events occur, but rather the types of explanation that individuals make.
    Dysfunctional explanations are more likely to occur the more negative or severe the event is.
    The focus should be on

    • The causes of events
    • How an individual perceives the consequences
    • How the events impact on important domains or areas of investment
    • And so on
  • Most models are diathesis-stress models in which a pre-existing vulnerability factor has interacted with subsequent stressors to produce the particular disorder
    It seems more likely that we will need different models and different weightings of factors to account for the onset of a first episode of an emotional disorder, maintenance and recovery, relapse, and future recurrence
  • An adequate cognitive account of emotion requires at least two levels of semantic representation
  • Emotional thinking should not be equated with irrational thinking.
  • Theories that have predicted global cognitive biases or that have searched for global vulnerability factors in the emotional disorders need to be revised. More specific biases are implicated.
  • The idea of loops and locked systems has become more evident in models of the emotional disorders
  • The cognitive and social-cognitive theories have highlighted the importance of social factors in the emotional disorders
  • An adequate model of mental functioning must be able to account for a range of inhibitory phenomena in relation to emotion.
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A contemporary learning theory perspective on the etiology of anxiety disorders: It’s not what you thought it was - a summary by an article by Mineka, & Zinbarg

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A contemporary learning theory perspective on the etiology of anxiety disorders: It’s not what you thought it was
Article by: Mineka, S. & Zinbarg, R. (2006)
American Psychologist, 61, 10-26


Specific phobia  

Individuals with specific phobias show intense and irrational fears of certain objects or situations that they usually go to great lengths to avoid.

Vicarious conditioning of fears and phobias

Strong and persistent phobias can be learned rapidly through observation alone.

Sources of individual differences in the acquisition of fears and phobias

Many individuals who do undergo traumatic experiences do not develop phobias. From a diathesis-stress perspective, such findings are expected. There seems to be a modest genetically based vulnerability for phobias. This genetic vulnerability may well be mediated through genetic contributions to fear conditioning, which may in turn be mediated through personality variables such as high treat anxiety that also seem to serve as vulnerability factors, affecting the speed and strength of conditioning.

Differences in life experiences among individuals can also strongly affect the outcome of conditioning experiences. Such experiential factors may serve as vulnerability (or invulnerability) factors for the development of phobias. The relevant differences in life experiences may occur before, during, or following a fear-conditioning experience, and they can act singly or in combination to affect how much fear is experienced, acquired, or maintained over time.

Impact of prior experiences

Latent inhibition demonstrates that simple prior exposure to a conditioned stimulus (CS) before the conditioned and unconditioned stimulus (US) are ever paired together reduces the amount of subsequent conditioning to the CS when paired with the US.

A person’s history of control over important aspects of his or her environment is another important experiential variable strongly affecting reactions to frightening situations. A greater sense of mastery and control may lead to a more readily adaption to frightening events and novel anxiety-provoking situations.

Impact of contextual variables during conditioning

Several different features of conditioning events themselves have a strong impact on how fear is acquired. Having control over a traumatic event (such as being able to escape it) has a major impact on how much fear is conditioned to CSs paired with that trauma. Far less fear is conditioned when the aversive event is escapable than when it is not.

Impact of postevent variables

Different kinds of experiences that people can have following conditioning affect the strength of the conditioned fear that is maintained over time. A person who is exposed to a more intense traumatic experience (not paired with the CS) after conditioning of a mild fear is likely to show an increase in

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Maximizing exposure therapy: An inhibitory learning approach - a summary of an article by Craske, Treanor, Conway, Zbozinek & Vervliet

Maximizing exposure therapy: An inhibitory learning approach - a summary of an article by Craske, Treanor, Conway, Zbozinek & Vervliet

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Maximizing exposure therapy: An inhibitory learning approach
An article by: Craske, M. G., Treanor, M., Conway, C. C., Zbozinek, T., & Vervliet, B. (2014).
Behaviour Research and Therapy, 58, 10-23


Inhibitory learning model of extinction

In a Pavlovian conditioning model, a neutral stimulus (conditional stimulus, CS) is followed by an aversive stimulus (unconditional stimulus, US). After a number of parings, the CS will come to elicit anticipatory fear reactions (conditional response, CR). The CR is presumed to depend upon the CS becoming a reliable predictor of the US. An association is posited between the memory representations of the CS and the US such that presentations of the CS will indirectly activate the memory of the US.

One powerful way to reduce conditional fear reactions is through extinction, in which the CS is repeatedly presented in the absence of the US.

Inhibitory learning is regarded as being central to extinction, although additional mechanisms, such as habituation, are likely to be involved. Inhibitory learning models mean that the original CS-US association learned during fear conditioning is not erased during extinction, but rather is left intact as new, secondary inhibitory learning about the CS-US develops, specifically that the CS no longer predicts the US.

The amygdala, which is particularly active during fear conditioning, appears to be inhibited by cortical influences identified as occurring from the medial prefrontal cortex as a result of extinction learning. After extinction, the CS possesses two meanings: 1) Its original excitatory meaning (CS-US). 2) an additional inhibitory meaning (CS-no US)

Even though fear subsides with enough trials of the CS in the absence of the US, retention of at least part of the original association can be uncovered by various procedures, which each one showing a continuing effect of the original excitatory association after extinction. 1) Conditional fear shows spontaneous recovering. 2) The strength of the CR increases in proportion to the amount of time since the end of extinction. 3) Renewal of conditional fear occurs if the surrounding context is changes between extinction and retest 4) Fear extinction appears to be specific to the context in which extinction occurs 5) Reinstatement of conditional fear occurs if unsignaled (or unpaired) US presentations occur between extinction and retest. 6) Rapid reacquisition of the CR is seen if the CS-US pairings are repeated following extinction

Deficits in inhibition and

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Tackling maladaptive memories through reconsolidation: From neural to clinical science - a summary of an article by Elsey& Kindt (2017).

Tackling maladaptive memories through reconsolidation: From neural to clinical science - a summary of an article by Elsey& Kindt (2017).

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Tackling maladaptive memories through reconsolidation: From neural to clinical science
By: Elsey, J. W. B. & Kindt, M. (2017).
Neurobiology of Learning and Memory, 142, 108-117

Memory reactivation can induce a labile period, during which previously consolidated memories are sensitive to change, and in need of restabilization. This is reconsolidation.
Memory labilization appears to result from the interplay of learning history, reactivation, and individual differences.


Memory reconsolidation

The dominant model of memory formation proposes that memories transition from a short-term and relatively unstable trace to a more persistent long-term form.
This transition from short-term memory to long-term memory is consolidation.
Consolidation is thought to be mediated by protein synthesis dependent synaptic changes.
Protein synthesis inhibitors (PSIs) prevent the expression of long-term memory when administered shortly after learning.
Once consolidated, memories appear insensitive to protein synthesis inhibition, and can prove highly recalcitrant to attempts at modification.

Reactivation of a memory can render it vulnerable to amnestic interventions.
Protein synthesis inhibition shortly after reactivation can prevent the later expression of long-ter memory.
Under certain conditions, a consolidated memory can be brought into a labile state by reactivation, during which the memory trace can be modified or even disrupted.
This labile state requires restabilization in a manner similar to consolidation.
The reactivation-induced period of lability is temporary.

The amnesia for auditory fear conditioning could be induced by the systemic administration of propranolol, timed to coincide with memory reactivation.
The blockade of beta-adrenergic receptors by propranolol is believed to indirectly inhibit protein synthesis by halting noradrenaline-stimulated CREB phosphorylation in the amygdala.

The disruption of reconsolidation by pharmacological means has been proven effective in both non-human animals and humans under controlled laboratory settings.

Reactivation and reconsolidation are not synonymous

Reconsolidation is most reliably induced by memory reactivations that in some way add to or indicate the need to update the memory.

Memory expression appears to be unnecessary for inferring memory reconsolidation.
NMDA receptor activation is necessary for the labiliation of a fear memory trace upon reactivation.
AMPA receptors are crucial for the expression of that memory.
These two processes are dissociable.

It is the prediction error, not the absence of reinforcement, that is necessary for the destabilizaiton of conditioned fear memories.

For the translation of reconsolidation-based research into clinical practice, simply generating a fear response or reactivating a patient’s memory may not trigger reconsolidation of the target memory trace.
An optimal reactivation session should involve some kind of prediction error.
Prediction errors could

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Is depression an adaptation? - summary of an article by Nesse

Is depression an adaptation? - summary of an article by Nesse

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Is depression an adaptation?
Article by: Nesse, R. M. (2000)
Archives of General Psychiatry, 57, 14-20


Abstract

In difficult situations, pessimism and lack of motivation may give a fitness advantage by inhibiting certain actions, especially:

  • Futile or dangerous challenges to dominant figures
  • Actions in the absence of a crucial resource or a viable plan
  • Efforts that would damage the body
  • Actions that would disrupt a currently unsatisfactory major life experience when it might recover or the alternative is likely to be even worse.

Introduction

Here are three causes for manifestations of disease

  • Manifestations that arise directly from a defect in the body’s machinery
    Have no utility
  • Defences or dysregulations of defences
    These are adaptations shaped by natural selection
  • Dysregulated or extreme defences

Correcting a defect is almost always useful, but blocking a defence can be harmful.

Global evidence

Depression is painful and interferes with normal function.
Other useful capacities such as pain, nausea and fatigue, are also aversive and disruptive.
Their very aversiveness is likely a product of natural selection, probably because they promote escape and avoidance of situations that decrease fitness.
From that perspective, the intrinsic aversiveness of most low mood and depression suggest that they may be related to defence.

The epidemiology of mood disorders.
If depression were rare, and had symptoms unrelated to the experiences of most people, this would suggest it was a disease unrelated to any defence.
But this issn’t the case.
There is no point of rarity in the distribution that can differentiate pathologic from non-pathologic depression.
The incidence of depression is highest at the ages where reproductive value peaks, a pattern characteristic of few diseases.

Defences are regulated by cues associated with situations in which they are useful, defects are not.
The regularity of the relationship between loss and negative affect and the proportionality of low mood to the magnitude of a loos imply that mood is regulated.
The relationship of depression to events is less consistent. This suggests that many depressive episodes are not defences.

Possible functions of low mood and depression

Signalling benefits of several kinds have been attributed to low mood or

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Genotype–environment correlations: Implications for determining the relationship between environmental exposures and psychiatric illness - summary of an article by Jaffee and Price

Genotype–environment correlations: Implications for determining the relationship between environmental exposures and psychiatric illness - summary of an article by Jaffee and Price

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Genotype–environment correlations: Implications for determining the relationship between environmental exposures and psychiatric illness
By: Jaffee, S. R., & Price, T. S. (2008)
Psychiatry, 7, 496–499


Abstract

Psychological risk factors for psychiatric illness are moderately heritable.
This has two implications

  • Individuals actively shape their environments through heritable behaviour
  • The relationship between environmental exposure and psychopathology may be confounded by genotype

There are three types of genotype-environment correlation

  • Passive
    The association between the genotype a child inherits from his or her parents and the environment in which the child is raised.
  • Evocative (or reactive)
    The association between an individual’s genetically influenced behaviour and others’ reactions to that behaviour.
  • Active (or selective)
    The association between an individual’s genetic propensities and the environmental niches that individual selects.

These forms of genotype-environment correlation differ from gene-environment interaction (GxE), which refers to genetic differences in sensitivity to particular environmental effects.

  • Genotype-environment correlations explain why individuals have a genetic propensity to engage in sensation-seeking behaviours affiliate with drug-abusing peers.
  • GxE explains why heavy drug use is most likely to lead to psychosis only among individuals with a particular genotype.

Evidence from the quantitative genetic literature

Twin and adoption studies demonstrated that putative environmental measures are heritable.
These include many environments that are associated with psychiatric illness, including:

  • Marital quality
  • Social support
  • Parental discipline and warmth
  • Family environment
  • Peer relationships
  • Desirable and undesirable life events
    • Divorce
    • Exposure to trauma

The weighted heritability of these environments ranges from 6 to 39%, with most ranging from 15 to 35%.

When a study involves child twins reporting their experiences, genetic influences on the putative environment reflect the extent to which the child’s genetic propensities elicit or evoke that experience.
When studies involve samples of adult twins reporting their experiences, genetic influences on the putative environment reflect the extent to which the adult’s genetic propensities modify or create that experience.

Environments are heritable because genotype influences the behaviours that evoke, select, and modify features of the environment.
Environments less amenable to behavioural modification tend to be less heritable.

Evidence from the molecular genetic literature

Molecular studies measure genotype directly.
It may be possible to identify specific genotypes that correlate with environmental variables.

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The subjective experience of emotion: A fearful view - summary of an article by LeDoux and Hofmann (2018)

The subjective experience of emotion: A fearful view - summary of an article by LeDoux and Hofmann (2018)

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The subjective experience of emotion: A fearful view. 
LeDoux, J. E. & Hofmann, S. G (2018)
Current Opinion in Behavioral Sciences, 19, 67–72.
doi:10.1016/j.cobeha.2017.09.011.


Abstract

The subjective emotional experience, the feeling, is the essence of an emotion.
Objective manifestations in behaviour and in body or brain physiology are, at best, indirect indicators of these inner experiences.
The most direct way to assess conscious emotional feelings is through verbal self-report.

Because behavioural and physiological responses are important contributors to emotions, and the circuits underlying these are highly conserved, studies of animals have an important role in understanding how emotions are expressed and regulated in the brain.

Measuring subjective experiences

Scientific assessments of inner experiences require some form of self-reporting.
People can typically give either a verbal or a nonverbal report of information to which they have introspective access, but cannot provide a verbal report of information that is only processed non-consciously.

Verbal self-report remains the gold standard in studies of consciousness.
It is most suitable for assessing the content of immediate experiences rather than remembered experiences.
It is less useful for assessing the motivations underlying actions.

Contemporary views of subjective emotional experiences in relation to brain circuits

The neuro-Darwinian Approach: subjective fear is an innate state of mind inherited from animal ancestors

Darwin defined emotions as innate ‘states of mind’ that humans have inherited from animal ancestors, and that, when aroused, cause the expression of so-called emotional behaviours.

Neuroscience proponent
Views emotions as subjective feelings that emerge from a subcortical neural circuit that is highly conserved across mammals, including humans.
The circuit is centered on the amygdala and related subcortical areas.
The amygdala circuit, when activated by a threat to well being, both gives rise to fearful feelings and controls innate behaviours and supporting physiological responses that help the organism defend against harm.
Cognitive elaboration of subcortical fear by higher-cortical prefrontal circuits makes possible introspection and verbal reports of fear in humans. The core of fear is the inherited mental state arising from the subcortical circuit.

Problematic for this view is the evidence suggesting that the experience of fear is not embodied in the amygdala.
The amygdala can respond to threats without the person knowing the threat is present and without feeling fear.
Also, fear can be experienced when the amygdala is damaged.

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Social anxiety disorder: A critical overview of neurocognitive research - a summary of an article by Cremers & Roelofs

Social anxiety disorder: A critical overview of neurocognitive research - a summary of an article by Cremers & Roelofs

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Social anxiety disorder: A critical overview of neurocognitive research.
Cremers, H. R., & Roelofs, K. (2016).
WIREs Cognitive Science, 7, 218-232
doi: 10.1002/wcs.1390


Abstract

Social anxiety disorder is a common disorder characterized by a persistent and excessive fear of one or more social or performance situations.
Behavioural inhibition is one of the early indicators of social anxiety and may advance into a certain personality structure and the development of maladaptive cognitive biases.

Several large-scale brain networks related to emotion, motivation, cognitive control, and self-referential processing have been identified, and are affected in social anxiety.
Social anxiety is also characterized by increased cortisol response and lower testosterone levels.
These neuroendocrine systems are related to altered connectivity patterns.

Introduction

Social anxiety disorder (SAD) is characterized by a persistent fear of one or more social or performance situations with exposure to unfamiliar people or to possible scrutiny by others.
A person with SAD fears that he or she will act in a way that will be humiliating or embarrassing.
Expose to the feared situations  almost invariably provokes anxiety.
Social situations are either avoided or endured with intense anxiety or distress.

Development, cognition, and treatment

The diagnosis of SAD requires that the condition interferes substantially with the person’s normal routine.

Research on personality traits and the development of social anxiety stresses the dimensional nature of social anxiety.
Traits related to emotional processing, much as neuroticism and extraversion are critical.

  • Neuroticism
    Regarded as a vulnerability marker in the development of SAD
  • Extraversion
    Regarded a ‘protective’ factor in the development of SAD

The heritability of social anxiety can, to a large extend, be explained by the heritability of these personality traits.

The relationship between personality factors and (social) anxiety development may be interpreted in a merely probabilistic manner.
Personality traits may simply capture some aspects of (social) anxiety and therefore naturally show covariation.

A three-factor solution for social anxiety

  • Social interaction fears
  • Observation fears
  • Public speaking fears

Such factors just pertain to the population, not the individual.

Developmental and cognitive models

Behavioural inhibition (BI): a temperamental trait referring to reactions of a child when confronted with novel situations and unfamiliar people.
One of the earliest developmental indications of social anxiety.

During the course of a child’s development, social anxiety may progress from such initial behavioural indicators, to increasing levels of self-consciousness and

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Hormones and psychiatric disorders - summary of part of Why zebras don't get ulcers: The acclaimed guide to stress, stress-related diseases, and coping-now revised and updated by Sapolsky

Hormones and psychiatric disorders - summary of part of Why zebras don't get ulcers: The acclaimed guide to stress, stress-related diseases, and coping-now revised and updated by Sapolsky

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Why zebras don't get ulcers: The acclaimed guide to stress, stress-related diseases, and coping-now revised and updated
By: Sapolsky, R. M. (2004).
New York: Henry Holt.


The hormones of the stress-repsonse

As the master gland, the brain can experience or think of something stressful and activate components of the stress-response hormonally.
Some of the hypothalamus-pituitary-peripheral gland links are activated during stress, some inhibited.

Two hormones vital to the stress-response released by the sympathetic nervous system:

  • Epinephrine
  • Norepinephrine
    Acts within seconds

Another important class of hormones in the response to stress are called glucocorticoids.
These are steroid hormones secreted by the adrenal gland.
Back the epinephrine activity up over the course of minutes to hours.

Because the adrenal gland is basically witless, glucocorticoid release must ultimately be under the control of the hormones of the brain.
When something stressful happens or you think a stressful thought, the hypothalamus secretes an array of releasing hormones into the hypothalamic-pituitary circulatory system that gets the ball rolling.
The principal such releaser is CRH (coticotropin releasing hormone).
A variety of minor players synergize with CRH
Withing fifteen seconds, CRH triggers the pituitary to release ACTH (corticotrpin) in the bloodstream.
ACTH reaches the adrenal gland and (in a few minutes) triggers glucocorticoid release.

Together, glucocorticoids and the secretions of the sympathetic nervous system (epinephrine and norepinephrine) account for a large percentage of what happens in your body during stress.

In times of stress, your pancreas is stimulated to release a hormone called glucagon.
Glucocorticoids, glucagon, and the systematic nervous system raise circulating levels of the sugar glucose.
These hormones are essential for mobilizing energy during stress.
Other hormones are activated as well.
The pituitary secretes prolactin, which plays a role in suppressing reproduction during stress.
Both the pituitary and the brain secrete endorphins and enkephalins, which help blunt pain perception.
The pituitary secretes vasopressin (antidiuretic hormone), which plays a role in the cardiovascular stress response.

Various hormonal systems are inhibited during stress
The secretion of various reproductive hormones such as estrogen, progesterone, and testosterone are inhibited.
Hormones related to growth are also inhibited.
As are the secretin of insulin.

A few complications

Fight or flight response is a way of conceptualizing the stress-response as preparing the body for that sudden burst of energy demands.
This might be different in females.
In most species, females are typically less aggressive than males, and having dependent young often precludes the option of flight.
Some suggest that the female stress-response is about

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Cortisol stress reactivity across psychiatric disorders: A systematic review and meta-analysis - summary of an article by Zorn. et al (2017)

Cortisol stress reactivity across psychiatric disorders: A systematic review and meta-analysis - summary of an article by Zorn. et al (2017)

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Cortisol stress reactivity across psychiatric disorders: A systematic review and meta-analysis
Zorn, J. V., Schür, R. R., Boks, M. P., Kahn, R. S., Joëls, M., & Vinkers, C. H. (2017)
Psychoneuroendocrinology, 77, 25–36.
doi:10.1016/j.psyneuen.2016.11.036


Introduction

The hypothalamus-pituitary-adrenal (HPA) axis and its end product cortisol are essential for an adequate response to stress.
A dynamic cortisol response, marked by a rapid rise and decline in cortisol levels following stress, is thought to be adaptive and to facilitate adequate coping with perceived threats in the environment.
Changes in cortisol stress reactivity may increase susceptibility to the negative effects of stress.

Prolonged, excessive or insufficient activation of the HPA axis may lead to changes in the brain and may subsequently result in the development of psychiatric disorders.

Discussion

 There are sex-specific changes in cortisol stress reactivity for MDD and anxiety disorders.
Women with current MDD or an anxiety disorder exhibit a blunted cortisol stress response compared with healthy controls.
Men with current MDD or SAD show an elevated cortisol response.

For schizophrenia, the cortisol response to psychosocial stress is blunted in both male and female patients.

Influence of sex and sex hormones

Sex is an important factor when studying cortisol stress reactivity across psychiatric disorders.

Women in the luteal phase of the menstrual cycle have a similar cortisol response as men, while women in the follicular phase, menopause and those using oral contraceptives show blunting of the cortisol response.

Higher testosterone levels were associated with lower cortisol responses in men and higher progesterone levels had the same effect in women.

Despite the rise of sex hormones in response to acute stress, baseline levels of testosterone, estradiol and progesterone could partially explain sex differences in cortisol stress reactivity.

The cortisol stress response as a resilience marker

There is a dynamic cortisol stress response in relation to psychiatric illness.
The response was altered in patients with current MDD or an anxiety disorder.

Recurrent episodes of MDD change the cortisol response more permanently.

Women with current MDD or an anxiety disorder exhibit a blunted cortisol response to psychosocial stress compared to healthy controls.
Male patients with current MDD or SAD show an elevated cortisol response to psychosocial stress.

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Cognitive theories of emotion - summary of chapter 3 of Cognition and emotion: form order to disorder

Cognitive theories of emotion - summary of chapter 3 of Cognition and emotion: form order to disorder

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Cognition and emotion: form order to disorder
Power, M & Dalgleish, T (2015)
Chapter 3
Cognitive theories of emotion


Introduction

Two main groups of theories

  • The associationist tradition
    Based on semantic networks
  • The constructivist position
    Appraisal theories

The starting point for the theories to be presented is an attempt to provide a cognitive account of normal emotions.

Zajonc argued that the initial procession of stimuli assesses the affective tone of the stimulus as positive or negative, safe or threatening, and that ‘cognitive’ processes occur subsequent to this affective processing.

Categorical versus dimensional approaches to emotion

Dimensions

There have been several related proposals that have focused on dimensions such as valance and arousal.

Subsequent theories have divided up the dimensions of valence and arousal.
Gray argued that the arousal system is in fact two separate systems

  • The behavioural activation system
  • The behavioural inhibition system
  • Over-activity and/or underactivity in either leads to different emotional consequences

Watson argued that the Valence dimension should be divided into two separate orthogonal dimensions, one of which is positive and the other negative (instead of bipolar)

Although studies of self-reported emotion and affect have been taken to support the dimensional structure of emotion (with most support for two separate dimensions of Valence and Arousal), there are a number of short-comings of these studies in relation to measurement problems.

Basic emotions

Basicness means that there is a small handful of core human emotions.
This provides a framework within which to divide up, integrate and organize the confusion of our emotional experience.
Also provides a way into other important approaches to emotions (such as evolution) and the foundations for a bridge between the study of human emotions and research into the emotional experiences of other species.

A formulation of the basic emotion debate in terms of the philosophy of emotion

The concept of emotion includes an event, a perception or interpretation, an appraisal, physiological change, a propensity for action, and conscious awareness.

Emotion as a paradigm could embrace overt

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Cognitive theories of emotional disorder - summary of chapter 4 of Cognition and emotion: from order to disorder

Cognitive theories of emotional disorder - summary of chapter 4 of Cognition and emotion: from order to disorder

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Cognition and emotion: from order to disorder
Power, M. & Dalgleish, T. (2015).
Chapter 4 
Cognitive theories of emotional disorder


Introduction

There are a number of influential cognitive approaches toe motion that have their starting points to be disorders of emotion.

Cognitive approaches to the emotional disorders have typically focused on a specific disorder.
This carving up of the emotional disorders can lead to a false sense of disjointedness between the emotions in comparison to the more over-arching theories.

Seligman’s learned helplessness theory

Learned helplessness

The role of perceived non-contingency plays an important role in the theory of learned helplessness.
The original theory focused on the key features of passivity and helplessness in the face of future events characteristic of depression.

Reformulated learned helplessness

Abramson added Weiner’s attribution theory to the original learned helplessness approach.
Although helplessness continued to be seen to arise from the perception of uncontrollability, the subsequent effects were now seen to depend both on the type and the importance of the event experienced, together with the explanation that the individual produced for the cause of the event.

The explanatory style dimensions focused on three of Weiner’s attributional dimensions

  • Internal-external or locus
    Whether the cause is seen to be due to something about the individual (internal) or due to something about other people or circumstances (external)
  • Stable-unstable
    Whether the cause is due to something that would recur future similar events
  • Global-specific
    Whether the cause influences only one area of the individual’s life or many

The combination of these dimensions led to the proposal that the emotional, motivational and cognitive deficits seen in depression could be accounted for by a particular set of attributions following the occurrence of a negative event.

The crucial type of attribution style that is identified as a vulnerability factor for depression is if the individual makes internal-stable-global attributions for the causes of negative events and external-unstable-specific attributions for positive events.
An internal attribution for a negative event leads to low self-esteem, especially if other individuals are perceived not to be helpless in such a situation (personal helplessness).
The additional stable and global attributions for negative evens add to the chronicity and the generality of the deficits observed in depressed individuals.

It is possible that depressogentic implicit attributional tendencies are not being detected by the routine

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A cognitive approach to panic - summary of an article by Clark (1986)

A cognitive approach to panic - summary of an article by Clark (1986)

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A cognitive approach to panic
Clark, D. M. (1986).
Behaviour Research and Therapy, 24, 461-470.


Abstract

Within this cognitive model, panic attacks are said to result from the catastrophic misinterpretation of certain bodily sensations. The sensations which are misinterpreted are mainly those involved in normal anxiety responses but also include other sensations. The catastrophic misinterpretation involves perceiving these sensations as much more dangerous than they really are.

The phenomenology of panic attacks

A panic attack consists of an intense feeling of apprehension or impending doom which is of sudden onset and which is associated with a wide range of distressing physical sensations. Panic attacks occur in both phobic and non-phobic anxiety disorders.

A cognitive model of panic attacks

It is proposed that panic attacks result from the catastrophic misinterpretation of certain bodily sensations. The sensations which are misinterpreted are mainly those which are involved in normal anxiety responses. The misinterpretation is perceiving these sensations as much more dangerous as they really are.

A wide range of stimuli can provoke a panic attack. These stimuli can be external and internal. If these stimuli are perceived as a threat, a state of mild apprehension results. This state is accompanied by a wide range of body sensations. If these anxiety-produced sensations are interpreted in a catastrophic fashion, a further increase in apprehension occurs, which produces a further increase in body sensations.

In the case of an ‘out of the blue’ panic attack, the trigger often seems to be the perception of a bodily sensation which itself is caused by a different emotional state or for example caffeine.

Other sensations than bodily sensations can also play a role in panic, particularly as triggering stimuli. Like the interpretation of mental processes.

 

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Modification of information processing biases in emotional disorders: Clinically relevant developments in experimental psychopathology - summary of an article by Baert, Koster and de Raedt (2011)

Modification of information processing biases in emotional disorders: Clinically relevant developments in experimental psychopathology - summary of an article by Baert, Koster and de Raedt (2011)

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Modification of information processing biases in emotional disorders: Clinically relevant developments in experimental psychopathology
Baert, S., Koster, E. H. W., De Raedt, R. (2011)
International Journal of Cognitive Therapy, 4, 208-222


Abstract

Experimental psychopathology has provided abundant evidence to suggest information-processing biases in anxiety and depression.

Cognitive bias modification (CBM) procedures are specifically designed to modify dysfunctional processing for those circumstances where patients are depleted form intentional control to override the bias. Through repeated practice, CBM intends to alter former biases and automate new, more adaptive cognitive processes. It holds potential in the treatment of anxiety and depression.

Cognitive theories on information processing

Research on information-processing in emotional disorders has predominantly been guided by the cognitive schema theory proposed by Beck and Bower’s associative network theory.

Beck’s cognitive schema theory.
Information-processing is guided by schema’s, defined as memory structures which, based on previous experiences, contain and organize information about the self, the world, and the future These schema’s are thought to bias encoding of information. Specific information processing biases at the level of attention, interpretation, and memory mediate incoming information and subjective experience. Eventual experience is considered to be the product of both bottom-up processing of the environment as well as top-down processing involving selection, abstraction, interpretation and elaboration. In the case of anxiety and depression, emotional information-processing will influence experience in a negative way, causing maladaptive emotional responses. These negative experiences further reinforce the maladaptive schemas.

It is thought that the active ingredients of cognitive behavioural therapy (CBT) act through modification of maladaptive cognition. Mostly, these techniques work by identifying maladaptive beliefs and negative thoughts and substituting these more adaptive ideas. CBT emphasizes the presence and content of schema-incongruent information that disconfirms former beliefs, which subsequently leads to new experiences that evoke or strengthen more adaptive schema’s.

The reciprocal influence between CBT and information processing bias has received scare attention. Information-processing biases may act as a barrier in CBT.

Information processing biases often act involuntarily and occur outside of conscious awareness. Although a change in controlled processing can lead to a change in automatic processing, this would require fulfilment of a least two crucial conditions. These are: 1) Using effortful control in situations of stress and negative mood. But, cognitive resources might not be sufficiently available. And 2) The individual must be motivated to do so. One possible direction is to include procedures modifying biases that are out of the patient’s voluntary control.

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Attention - summary of (part of) chapter 2 of Cognitive behavioural processes across psychological disorders: A transdiagnostic approach to research and treatment

Attention - summary of (part of) chapter 2 of Cognitive behavioural processes across psychological disorders: A transdiagnostic approach to research and treatment

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Cognitive behavioural processes across psychological disorders: A transdiagnostic approach to research and treatment
Harvey, A., G., Watkins, E., Mansell, W., Shafran, R. (2004)
Chapter 2
Attention


What is selective attention?

Out experience at any one point is dominated by some stimuli at the expense of others.
Selective attention is a process by which specific stimuli, within the external and internal environment, are selected for further processing.
Further processing may be reasoning, thought, or the generation of a plan of action. These processes are not to be confused with selective attention itself.
Selective attention is the internal filtering of stimuli. S

Attentional bias: a systematic tendency to attend (or avoid attending) to a particular class of stimuli.

The processes of selective attention have been divided into

  • Automatic processes
    The person is either unaware that their attention has been drawn to a particular stimulus, or they may feel that their attention is out of their own control.
  • Controlled processes
    Consciously planning to attend a stimulus.

This might be a continuum.

Most everyday behaviours are triggered, and often maintained, in an automatic manner such that they free up resources and thereby maximize the efficiency with which we operate the world.

Self-focused attention

Self-focused attention is an awareness of self-referent, internally generated information that stands in contrast to an awareness of externally generated information derived through sensory receptors.
Self-focused attention includes awareness of

  • Physical state
  • Feelings
  • Thoughts
  • Emotions
  • Memories

How is selective attention measured?

Self-report measures

Asking people.
Self-report measures index how much the individual reports attending to the stimulus identified.

Advantages

  • Easy to use in clinical practice where other methods may not be available
  • Attention to certain stimuli may be difficult to address in other ways

Drawbacks to self-report

  • They tend to tap a broad range of processes other than attention
  • Self-report scales are prone to biases and inaccuracies in memory because they are completed retrospectively
  • They cannot provide information about automatic processes that are too quick or subtle for the person to notice

The emotional stroop task

It has been proposed that the participants’ selective attention to the content of

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Thought - summary of (part of) chapter 5 of Cognitive behavioural processes across psychological disorders: A transdiagnostic approach to research and treatment

Thought - summary of (part of) chapter 5 of Cognitive behavioural processes across psychological disorders: A transdiagnostic approach to research and treatment

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Cognitive behavioural processes across psychological disorders: A transdiagnostic approach to research and treatment
Harvey, A., G., Watkins, E., Mansell, W., Shafran, R. (2004)
 
Chapter 5
Thought


Introduction

Metacognitive processes and beliefs: those concerned with the appraisal, monitoring or control of thinking itself

Intrusions

Intrusions are spontaneous, unwanted, unbidden, uncontrollable and discrete thoughts, images, or urges that are attributed to internal origins.
Many intrusive thoughts involve memories.

Normal and abnormal intrusions

Intrusions are normal and universal.
What distinguishes normal form abnormal intrusions is that clinical intrusions tend to be experienced as more intense, more uncomfortable, and less controllable.

Patients differ in their appraisals and responses to intrusions compared to controls.
They tend to view them as more meaningful and important, and are more likely to act in response to them.
Two particular responses to intrusions are unhelpful

  • Recurrently dwelling on them
  • Thought suppression

Forms of intrusions

Intrusions can occur in the form of

  • Verbal thought
  • Image
  • Urge

Images

Images are contents of consciousness that possess sensory qualities. They usually provide a perceptual-like analogue of some or all of the sensory aspects of a real-world experience.

Images are particularly potent at evoking emotional and physiological responses and at influencing the development of coping plans and the implementation of behaviour.
Verbal thoughts and images each influence and lead onto the other.

Urges

An urge is the internal experience of a desire to perform a particular act.
They can be induced by exposure to the object of the desire, contextual cues associated with the behaviour, emotional triggers and imagining performing an action or imagining a desired outcome.

Current concerns

The majority of psychological disorders are characterized by disorder-specific intrusive thoughts.

Intrusive thoughts are triggered by conditioned associations at either a sensory or a meaning level.
Stimulus or response cues associated with the content of the intrusion can trigger the intrusion.

Recurrent negative thinking: worry and rumination

One response to an intrusive thought is to further dwell on the subject matter of the intrusion, trying to work through or resolve it.
This is likely if the intrusion is

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Anxiety disorders in children and adolescents: Nature, development, treatment and prevention - summary of chapter F1 of e-Textbook of Child and Adolescent Mental Health.

Anxiety disorders in children and adolescents: Nature, development, treatment and prevention - summary of chapter F1 of e-Textbook of Child and Adolescent Mental Health.

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IACAPAP e-Textbook of Child and Adolescent Mental Health.
J. M. Rey (2018)
Chapter F.1
Anxiety disorders in children and adolescents: Nature, development, treatment and prevention.


Introduction

In the child and adolescent fields, there is a more common tendency to examine disorders as a whole.

Externalizing disorders are disorders in which people act out inner conflict or emotions. Internalizing disorders reflect problems with the self.

Description and diagnosis

The core feature of anxiety disorders is avoidance. In most cases, this includes overt avoidance of specific situations, places or stimuli. It may also involve subtle forms of avoidance such as hesitancy, uncertainty, withdrawal, or ritualized actions. The key difference between specific disorders is the trigger for this avoidance. The avoidance is generally accompanied by affective components of fearfulness, distress or shyness. Some children may have difficulty verbalising these emotions.

Anxiousness occurs due to an expectation that some dangerous or negative event is about to occur. In identifying the anxious child, it is crucial to determine that the avoidance occurs due to an expectation of some form of threat. All of the anxiety disorders will involve an anticipation of threat, which may take the form of worry, rumination, anxious anticipation, or negative thoughts. The key differences between disorders lie in the content of these beliefs. In addition to the beliefs, behaviours and emotions, anxious children will often report a range of associated physical complains reflecting heightened arousal. These are rarely specific to a given disorder.

Physical symptoms that are common among anxious children include: Headaches, stomach aches, nausea, vomiting, diarrhoea, and muscle tension. It is common for many anxious children to have difficulty with sleep.

Anxiety-related disorders

Children with obsessive compulsive disorder (OCD) report repetitive and intrusive thoughts, images or urges, often accompanied by repeated characteristic actions or behaviours with the goal of reducing anxiety. The mental components commonly focus on some expected threat or danger, although sufferers from some forms of OCD might focus more one a sense of disgust and a belief that certain actions simply ‘feel right’. When a threat expectation exists, the corresponding rituals are generally aimed at preventing or undoing the expected danger.

Many children are unable to clearly describe their beliefs and motivations.

Post-traumatic stress disorder involves a constellation of symptoms of heightened arousal, intrusions, detachment, and avoidance that occur following a severe event. Post-traumatic stress disorder is relatively infrequent in childhood.

School refusal

School refusal is not a formal diagnosis.

School refusal is not an anxiety disorder and may be motivated by many factors aside from anxiety.

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Depression in children and adolescents - summary of chapter E.1 of Textbook of Child and Adolescent Mental Health

Depression in children and adolescents - summary of chapter E.1 of Textbook of Child and Adolescent Mental Health

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IACAPAP e-Textbook of Child and Adolescent Mental Health.
J. M. Rey (2018)
Chapter E.1
Depression in children and adolescents

Epidemiology

Prevalence varies depending on the population, the period considered, informant, and criteria used for diagnosis. Most countries concur that about 1 to 2% of pre-pubertal children and about 5% of adolescents suffer from clinically significant depression at any one time. The cumulative prevalence (accumulation of new cases in previously unaffected individuals) is higher.

Gender and culture

The ratio of depression in males and females is similar in pre-pubertal children. It becomes about twice as common among females during adolescence.

Burden of illness

Depression poses a substantial burden to the individual suffering from this disorder and the society at large. Interpersonal relationships are particularly likely to suffer when someone is depressed. Depression is likely to progress into a chronic, recurring disease if not treated.

The burden of depression is increased because it appears to be associated with behaviours linked to other chronic diseases, although the nature of this association is unclear.

Age of onset and course

Depressed patients can display symptoms of depression at any age. The pattern varies slightly according to developmental stage.

Age at onset does not seem to define separate depressive subgroups. Earlier onset is associated with multiple indicators of greater illness burden in adulthood across a wide range of domains.

Adolescents often have a reactive affect and can, with effort, hide their symptoms.

Course

Clinical depression in youth follows a recurring course. An episode of depression in clinically referred patients last 7 to 9 months on average, but it can be shorter in non-referred community samples. Depressive episodes are, on average, a spontaneously remitting illness. Recurrence is high even after treatment.

Predictors of recurrence include: poorer response to treatment, greater severity, chronicity, previous episodes, comorbidity, hopelessness, negative cognition style, family problems, low socioeconomic status, and exposure to abuse or family conflict

Subtypes of depression

Different types of depression may have implications for treatment and prognosis.

Etiology and risk factors

The etiology of depression is complex, multifactorial, and the object of much academic argument.

Depression in youth appears to be the result of complex interactions between biological vulnerabilities and environmental influences. Biological vulnerabilities may result from children’s genetic endowment and form prenatal factors. Environmental influences include children’s family relationships, cognitive style, stressful life events, and school and neighbourhood characteristics.

Comorbidity

Comorbidity is the simultaneous occurrence of two or more distinct illnesses in the one individual. Depression comorbid with other disorders frequently in children and adolescents.

Berkson effect: comorbidity is particularly the cause in clinical settings because the likelihood of referral is a function of the combined likelihood of referral for each disorder individually.

Patients with comorbid disorders show greater impairment than those with a single diagnosis. It is also associated with worse adult outcomes.

Psychiatric disorders that often

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Interpersonal processes in social phobia - summary of an article by Alden & Taylor (2004)

Interpersonal processes in social phobia - summary of an article by Alden & Taylor (2004)

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Interpersonal processes in social phobia
Alden, L. E., & Taylor, C. T. (2004)
Clinical Psychology Review24(7), 857-882


Introduction

Social phobia involves anxiety-related symptoms and is an interpersonal disorder. It is a condition in which anxiety disrupts the individual’s relationships with other people.

Social anxiety is conceptualized and measured in somewhat different ways across various domains.

Interpersonal perspective

Interpersonal models share the assumption that good social relationships contribute to psychopathology. The self-perpetuating interpersonal cycle means that we tend to expect people in the present to treat us in the same way that people have in the past and we tend to repeat the behavioural strategies we learned to handle those earlier events. Our behaviour exerts a pull on other people that tends to evoke responses that maintain our social assumptions, expectations, and behavioural patterns.

Dysfunctional patterns are the result of an ongoing interaction between the individual and the social environment. This is a social developmental process that begins early and continues throughout the lifespan. Our relationships shape our sense of self and others.

Social anxiety disorder and social relationships

People with social anxiety disorder have fewer social relationships than other people.

Social anxiety is associated with a variety of dysfunctional strategies in relationships, including strategies of non-assertiveness and avoidance of emotional expression and conflict. Socially anxious people also reported over-reliance on others.

Even when people with social anxiety develop relationships, they view those relationships as less intimate, functional and satisfying than do people without social anxiety.

Self-perpetuating interpersonal cycles

Socially anxious people behave in ways that lead to negative social outcomes. People with social phobia may establish negative interpersonal cycles between themselves and others in which they adopt behavioural strategies that evoke negative reactions.

Behavioural patterns

The behaviours most commonly associated with social anxiety are: low social skill, non-assertiveness, visible anxiousness and some studies also found differences between socially anxious and non-anxious people on specific anxiety-related micro behaviours

Socially anxious individuals can appear less skilful and more anxious than other people.

Other researchers report evidence of critical or angry behaviour in socially anxious samples.

Others’ reactions

People with psychological problems often

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Interpersonal processes in depression - summary of an article by James, Hagan & Joiner (2013)

Interpersonal processes in depression - summary of an article by James, Hagan & Joiner (2013)

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Interpersonal processes in depression
James, J. L., Hagan, C. R., & Joiner, T. E. (2013)
Annual Review of Clinical Psychology9, 355-377


Abstract

Humans have an intrinsic need for social connection, so it is crucial to understand depression in an interpersonal context.

Interpersonal theories of depression posit that depressed individuals tend to interact with others in a way that elicits rejection, which increases the risk for future depression.

Introduction

Depression impacts how individuals interact with people in their environment. Some symptoms of depression are inherently likely to produce interpersonal distress and impairment. These symptoms could help maintain the current episode and create a troubled interpersonal context that could potentially trigger future episodes of depression.

Depression is persistent disorder within acute episodes.

Basic behavioural features and communication behaviours associated with depression

Differences have been identified are in: the amount of facial expression (more animated facial expressions to express sadness in depressed individuals), eye contact (less in depressed individuals), posture (depressed individuals hold their head downward and engage in more self-touching), non-verbal gestures (less in depressed individuals). The extent to which people demonstrate these deficits had been linked to the severity of their depressive state.

Following treatment or the remission of a major depressive episode, these behavioural features of depression tend to show improvement.

While communicating and interacting with others, depressed individuals have been found to speak more slowly and with less volume and voice modulation. Their voices have been perceived more negatively. They also produce a lesser number of social interpersonal actions. When they do interact, they tend to be much more negative in their chosen topics and self-disclosure negative feelings.

Social skills and depression

Depression is associated with social skills deficits. The social skills deficits that have been linked with depression may be a product of the basic behavioural features and communication behaviours that are associated with depression.

Social skills impairments have been viewed as more state-like than trait-like. Social skills deficits operate as a vulnerability to depression that only becomes problematic in the presence of a significant stressor.

The relationship between social skill deficits and later depression is mediated by the presence of relations with others.

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Familial and social environments in the etiology and maintenance of anxiety disorders - summary of an article by Hudson & Rapee (2009)

Familial and social environments in the etiology and maintenance of anxiety disorders - summary of an article by Hudson & Rapee (2009)

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Oxford handbook of anxiety and related disorders
Hudson, J. L., & Rapee, R. M. (2009)
Familial and social environments in the etiology and maintenance of anxiety disorders.


Introduction  

Factors in the individual’s environment are likely to provide understanding of why one vulnerable individual may develop anxiety disorder and another may not. It is an individual’s specific environment (non-shared) that accounts for the most environmental influence.

Individuals with specific genetic vulnerabilities may elicit particular environments. Individuals at genetic risk who are exposed to a relevant environmental factor may show an increased morbidity.

The role of the family in anxiety disorders

Parenting

There is a link between avoidance of threatening stimuli and the maintenance of anxiety disorders. Parenting behaviours that serve to accommodate or enhance avoidant strategies are likely to impact on the maintenance of anxiety disorders. They may also contribute to the development of anxiety disorders in individuals with an existing anxious vulnerability.

There is a positive relationship between the anxiety disorders and parenting that is controlling, overprotective, or lacking in autonomy granting. The ultimate consequence of overprotective parenting is that the child avoids potentially threatening situations and is prevented from potentially learning the situation is not as dangerous as predicted or she or he is able to exert some control in the situation.

There is some evidence that parenting high in negativity and rejection and low in warmth is also associated with anxiety disorders.

Temperamental factors interact with parent behaviour and play a role in eliciting overprotective parenting. An anxious child may elicit increased involvement and help from their environment. This increased help will serve to decrease the child’s autonomy and increase avoidance of novel anxiety-provoking situations and ultimately maintain the child’s vulnerability to anxiety.

Overprotection/control and rejection/negativity may reduce the child’s opportunity to approach novel situations and to experience confidence and independence.

Parents of anxious children are more likely to support avoidant responding to ambiguously threatening stimuli.

Summary

The key parenting variables that have been associated with anxiety disorders are parenting that is: overprotective/controlling and lacking autonomy granting, negative and lacking warmth and parenting that enhances the child’s avoidance of ambiguously threatening situations. These parenting variables are of most importance in the context of a temperamentally vulnerable child.

Family environment

There are a number of more general facets of the family environment that may be of interest in the development of anxiety disorders. These are cohesion, inter-parental conflict and stressful and negative family environments

There

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Using and finding summaries, study notes en practice exams on JoHo WorldSupporter

There are several ways to navigate the large amount of summaries, study notes en practice exams on JoHo WorldSupporter.

  1. Starting Pages: for some fields of study and some university curricula editors have created (start) magazines where customised selections of summaries are put together to smoothen navigation. When you have found a magazine of your likings, add that page to your favorites so you can easily go to that starting point directly from your profile during future visits. Below you will find some start magazines per field of study
  2. Use the menu above every page to go to one of the main starting pages
  3. Tags & Taxonomy: gives you insight in the amount of summaries that are tagged by authors on specific subjects. This type of navigation can help find summaries that you could have missed when just using the search tools. Tags are organised per field of study and per study institution. Note: not all content is tagged thoroughly, so when this approach doesn't give the results you were looking for, please check the search tool as back up
  4. Follow authors or (study) organizations: by following individual users, authors and your study organizations you are likely to discover more relevant study materials.
  5. Search tool : 'quick & dirty'- not very elegant but the fastest way to find a specific summary of a book or study assistance with a specific course or subject. The search tool is also available at the bottom of most pages

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Quicklinks to fields of study (main tags and taxonomy terms)

Field of study

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