What are therapeutic strategies for enhancing inhibitory learning?

Therapeutic strategies for enhancing inhibitory learning are:

Expectancy violation
The more the expectancy can be violated by experience, the greater the inhibitory learning
Deepened extinction
Either multiple fear CSs are first extinguished separately before being combined during extinction, or a previously extinguished cue is paried with a novel CS
Ocassional reinforced extinction
Occasional CS-US pairings during extinction training, this enhances the expectancy violation
Removal of safety signals
Variability
Exposure is conducted to items from the anxiety-hierarchy in random order
Retrieval cues
Cues of the CS-noUS association
Multiple contexts
Context renewal
Reconsolidation
Extinction during a reconsolidation window

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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
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
Deficits in inhibition and anxiety disorders
Inhibitory learning versus habituation and behavioural testing approaches to exposure
Therapeutic strategies for enhancing inhibitory learning and its retrieval
Therapeutic strategy for enhancing inhibitory regulation

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 anxiety disorders

The number of individuals who fail to achieve clinically

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Anxiety- and mood disorders

This is a bundle with information about anxiety- and mood disorders.
The bundle is based on the course anxiety- and mood disorders taught at the third year of

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

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
Social phobia
Panic disorder with and without agoraphobia
Posttraumatic stress disorder
Generalized anxiety disorder
Obsessive-compulsive disorder

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 fear with the CS.

A US revaluation process can occur when

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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
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
Deficits in inhibition and anxiety disorders
Inhibitory learning versus habituation and behavioural testing approaches to exposure
Therapeutic strategies for enhancing inhibitory learning and its retrieval
Therapeutic strategy for enhancing inhibitory regulation

Inhibitory learning model of extinction

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

Deficits in inhibition and anxiety disorders

The number of individuals who fail to achieve clinically

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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
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
Reactivation and reconsolidation are not synonymous
Prediction error, reconsolidation, and extinction

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 include not only the violation of expectations, but also the learning of

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

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

Abstract
Introduction
Global evidence
Possible functions of low mood and depression
In what situations is low mood useful?
Are the core aspects of depression ever useful?

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 depression.

Some suggest that depression in adults is a plea for help.

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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
By: Jaffee, S. R., & Price, T. S. (2008)
Psychiatry, 7, 496–499

Abstract
Evidence from the quantitative genetic literature
Evidence from the molecular genetic literature
Implications for disease prevention

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.
Significant genotype-environment correlations are relatively uncommon.

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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.
LeDoux, J. E. & Hofmann, S. G (2018)
Current Opinion in Behavioral Sciences, 19, 67–72.
doi:10.1016/j.cobeha.2017.09.011.

Abstract
Measuring subjective experiences
Contemporary views of subjective emotional experiences in relation to brain circuits
Conscious feelings in clinical assessment

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.
Medications can change behavioural responses to threats without changing the subjective feeling.

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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.
Cremers, H. R., & Roelofs, K. (2016).
WIREs Cognitive Science, 7, 218-232
doi: 10.1002/wcs.1390

Abstract
Introduction
Development, cognition, and treatment
Neurobiology
Neurodocrine circuitries
Discussion

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 preoccupation with peer feedback and exclusion.
Important elements

Low perceived

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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

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
The biology of depression
Psychiatric disorders and abnormal stress-responses

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 tend and befriend, taking care of her young and seeking social

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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
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
Discussion

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

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

Introduction
Categorical versus dimensional approaches to emotion
A formulation of the basic emotion debate in terms of the philosophy of emotion
The arguments for basic emotions
Toward a core set of basic emotions
Network theories
Other network theories
Appraisal theories
Arousal and motivation based appraisal theories
Cognitive appraisal theories
Summary

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 behaviour.

In philosophical terms, it is only meaningful to distinguish one emotion from

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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
Seligman’s learned helplessness theory
Beck’s cognitive therapy
Williams, Watts, MacLeod and Mathews (1988, 1997)
Teasdale and Barnard
Social-cognitive theories
Miscellaneous theories of emotional disorders
Summary

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

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

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

Abstract
The phenomenology of panic attacks
A cognitive model of panic attacks

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
Baert, S., Koster, E. H. W., De Raedt, R. (2011)
International Journal of Cognitive Therapy, 4, 208-222

Abstract
Cognitive theories on information processing
Attentional biases in depression and anxiety
On the causal status of information processing biases
Introducing cognitive bias modification of attentional bias
Toward a clinical application

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

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?
Self-focused attention
How is selective attention measured?
To what kind of stimuli do people selectively attend?
Do attentional processes play a causal role?
Theoretical issues
Clinical implications

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 the word interfered with their response to name the colour of the ink.

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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

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
Intrusions
Normal and abnormal intrusions
Current concerns
Recurrent negative thinking: worry and rumination
Discussion
Clinical implications

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 considered to be personally important.
The recurrent thinking, in response to a negative intrusion,

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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.

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
Description and diagnosis
Epidemiology
Assessment
Risk and maintaining factors

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. When it occurs, anxiety is a common underlying element. But, anxiety alone

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

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
Alden, L. E., & Taylor, C. T. (2004)
Clinical Psychology Review, 24(7), 857-882

Introduction
Interpersonal perspective
Social anxiety disorder and social relationships
Self-perpetuating interpersonal cycles
Social skill deficit or self-protective strategy
Cognitive processing of social information
Social pathogenesis
Self-perpetuating cycles
Variability in social learning experiences
Interpersonal processes in treatment

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 elicit negative responses from other people. There may be a presence of a global

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

Interpersonal processes in depression
James, J. L., Hagan, C. R., & Joiner, T. E. (2013)
Annual Review of Clinical Psychology, 9, 355-377

Abstract
Introduction
Basic behavioural features and communication behaviours associated with depression
Social skills and depression
Interpersonal feedback seeking and depression
Integrative models of excessive reassurance seeking and negative feedback seeking
Interpersonal styles and depression
Interpersonal consequences of depression

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)

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
The role of the family in anxiety disorders
Social relationships and anxiety disorders
Relationships and treatment outcome

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 is a causal link between inter-parental conflict and increased anxiety symptoms. There

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Anxiety and mood disorders, uva