What are therapeutic strategies for enhancing inhibitory learning?

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 fear with the CS.

A US revaluation process can occur when

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

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.
Significant genotype-environment correlations are relatively uncommon.

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 preoccupation with peer feedback and exclusion.
Important elements

• Low perceived

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.

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

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.

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

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

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