Neural mechanisms of the cognitive model of depression
TL;DR: The functional and structural neurobiological architecture of Beck's cognitive model of depression is identified and it is shown that in general the negative cognitive biases in depression are facilitated by increased influence from subcortical emotion processing regions combined with attenuated top-down cognitive control.
Abstract: In the 40 years since Aaron Beck first proposed his cognitive model of depression, the elements of this model — biased attention, biased processing, biased thoughts and rumination, biased memory, and dysfunctional attitudes and schemas — have been consistently linked with the onset and maintenance of depression. Although numerous studies have examined the neural mechanisms that underlie the cognitive aspects of depression, their findings have not been integrated with Beck's cognitive model. In this Review, we identify the functional and structural neurobiological architecture of Beck's cognitive model of depression. Although the mechanisms underlying each element of the model differ, in general the negative cognitive biases in depression are facilitated by increased influence from subcortical emotion processing regions combined with attenuated top-down cognitive control.
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TL;DR: This Review synthesizes recent data from human and rodent studies from which emerges a circuit-level framework for understanding reward deficits in depression, and discusses some of the molecular and cellular underpinnings of this framework, ranging from adaptations in glutamatergic synapses and neurotrophic factors to transcriptional and epigenetic mechanisms.
Abstract: Mood disorders are common and debilitating conditions characterized in part by profound deficits in reward-related behavioural domains. A recent literature has identified important structural and functional alterations within the brain's reward circuitry--particularly in the ventral tegmental area-nucleus accumbens pathway--that are associated with symptoms such as anhedonia and aberrant reward-associated perception and memory. This Review synthesizes recent data from human and rodent studies from which emerges a circuit-level framework for understanding reward deficits in depression. We also discuss some of the molecular and cellular underpinnings of this framework, ranging from adaptations in glutamatergic synapses and neurotrophic factors to transcriptional and epigenetic mechanisms.
1,365 citations
TL;DR: Although the precise mechanisms of plasticity are still not fully understood, moderate to severe stress appears to increase the growth of several sectors of the amygdala, whereas the effects in the hippocampus and prefrontal cortex tend to be opposite.
Abstract: Experiential factors shape the neural circuits underlying social and emotional behavior from the prenatal period to the end of life. These factors include both incidental influences, such as early adversity, and intentional influences that can be produced in humans through specific interventions designed to promote prosocial behavior and well-being. Here we review important extant evidence in animal models and humans. Although the precise mechanisms of plasticity are still not fully understood, moderate to severe stress appears to increase the growth of several sectors of the amygdala, whereas the effects in the hippocampus and prefrontal cortex tend to be opposite. Structural and functional changes in the brain have been observed with cognitive therapy and certain forms of meditation and lead to the suggestion that well-being and other prosocial characteristics might be enhanced through training.
625 citations
TL;DR: Human responses to stress and trauma vary widely; some people develop trauma-related psychological disorders, such as posttraumatic stress disorder (PTSD) and depression; others develop mild to moderate psychological symptoms that resolve rapidly; still others report no new psychological symptoms in response to traumatic stress.
Abstract: Human responses to stress and trauma vary widely. Some people develop trauma-related psychological disorders, such as posttraumatic stress disorder (PTSD) and depression; others develop mild to moderate psychological symptoms that resolve rapidly; still others report no new psychological symptoms in response to traumatic stress. Individual variability in how animals and humans respond to stress and trauma depends on numerous genetic, developmental, cognitive, psychological, and neurobiological risk and protective factors.
608 citations
TL;DR: An update on the validity and reliability of the CMS model, and recent data on the neurobiological basis of CMS effects and the mechanisms of antidepressant action are reviewed: the volume of this research may be unique in providing a comprehensive account of antidepressants action within a single model.
592 citations
Cites background from "Neural mechanisms of the cognitive ..."
...Broadly speaking, theories of depression have either a psychological or a neurobiological basis (though there are recent attempts to bring these two explanatory frameworks into alignment: e.g. Disner et al., 2011; Willner et al., 2013)....
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TL;DR: The updated theoretical model provides a framework for addressing significant questions regarding the phenomenology of disorders not explained in previous iterations of the original model.
Abstract: For over 50 years, Beck's cognitive model has provided an evidence-based way to conceptualize and treat psychological disorders. The generic cognitive model represents a set of common principles that can be applied across the spectrum of psychological disorders. The updated theoretical model provides a framework for addressing significant questions regarding the phenomenology of disorders not explained in previous iterations of the original model. New additions to the theory include continuity of adaptive and maladaptive function, dual information processing, energizing of schemas, and attentional focus. The model includes a theory of modes, an organization of schemas relevant to expectancies, self-evaluations, rules, and memories. A description of the new theoretical model is followed by a presentation of the corresponding applied model, which provides a template for conceptualizing a specific disorder and formulating a case. The focus on beliefs differentiates disorders and provides a target for treatme...
587 citations
Cites background from "Neural mechanisms of the cognitive ..."
...F or p er so na l u se o nl y. CP10CH01-Beck ARI 11 February 2014 7:10 Disner et al. 2011), future research may look toward integrating the GCM with biological processes (Forgeard et al. 2011)....
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04 Dec 1979TL;DR: Hollon and Shaw as discussed by the authors discuss the role of emotions in Cognitive Therapy and discuss the integration of homework into Cognitive Therapy, and discuss problems related to Termination and Relapse.
Abstract: 1. An Overview 2. The Role of Emotions in Cognitive Therapy 3. The Therapeutic Relationship: Application to Cognitive Therapy 4. Structure of the Therapeutic Interview 5. The Initial Interview 6. Session by Session Treatment: A Typical Course of Therapy 7. Application of Behavioral Techniques 8. Cognitive Techniques 9. Focus on Target Symptoms 10. Specific Techniques for the Suicidal Patient 11. Interview with a Depressed Suicidal Patient 12. Depressogenic Assumptions 13. Integration of Homework into Therapy 14. Technical Problems 15. Problems Related to Termination and Relapse 16. Group Cognitive Therapy for Depressed Patients Steven D. Hollon and Brian F. Shaw 17. Cognitive Therapy and Antidepressant Medications 18. Outcome Studies of Cognitive Therapy Appendix: Materials *The Beck Inventory *Scale for Suicide Ideation *Daily Record of Dysfunctional Thoughts *Competency Checklist for Cognitive Therapists *Possible Reasons for Not Doing Self-Help Assignments *Research Protocol for Outcome Study at Center for Cognitive Therapy *Further Materials and Technical Aids
9,970 citations
TL;DR: Notably, major depressive disorder is a common disorder, widely distributed in the population, and usually associated with substantial symptom severity and role impairment, and while the recent increase in treatment is encouraging, inadequate treatment is a serious concern.
Abstract: ContextUncertainties exist about prevalence and correlates of major depressive
disorder (MDD).ObjectiveTo present nationally representative data on prevalence and correlates
of MDD by Diagnostic and Statistical Manual of Mental Disorders,
Fourth Edition (DSM-IV) criteria, and on study
patterns and correlates of treatment and treatment adequacy from the recently
completed National Comorbidity Survey Replication (NCS-R).DesignFace-to-face household survey conducted from February 2001 to December
2002.SettingThe 48 contiguous United States.ParticipantsHousehold residents ages 18 years or older (N = 9090) who responded
to the NCS-R survey.Main Outcome MeasuresPrevalence and correlates of MDD using the World Health Organization's
(WHO) Composite International Diagnostic Interview (CIDI), 12-month severity
with the Quick Inventory of Depressive Symptomatology Self-Report (QIDS-SR),
the Sheehan Disability Scale (SDS), and the WHO disability assessment scale
(WHO-DAS). Clinical reinterviews used the Structured Clinical Interview for DSM-IV.ResultsThe prevalence of CIDI MDD for lifetime was 16.2% (95% confidence interval
[CI], 15.1-17.3) (32.6-35.1 million US adults) and for 12-month was 6.6% (95%
CI, 5.9-7.3) (13.1-14.2 million US adults). Virtually all CIDI 12-month cases
were independently classified as clinically significant using the QIDS-SR,
with 10.4% mild, 38.6% moderate, 38.0% severe, and 12.9% very severe. Mean
episode duration was 16 weeks (95% CI, 15.1-17.3). Role impairment as measured
by SDS was substantial as indicated by 59.3% of 12-month cases with severe
or very severe role impairment. Most lifetime (72.1%) and 12-month (78.5%)
cases had comorbid CIDI/DSM-IV disorders, with MDD
only rarely primary. Although 51.6% (95% CI, 46.1-57.2) of 12-month cases
received health care treatment for MDD, treatment was adequate in only 41.9%
(95% CI, 35.9-47.9) of these cases, resulting in 21.7% (95% CI, 18.1-25.2)
of 12-month MDD being adequately treated. Sociodemographic correlates of treatment
were far less numerous than those of prevalence.ConclusionsMajor depressive disorder is a common disorder, widely distributed in
the population, and usually associated with substantial symptom severity and
role impairment. While the recent increase in treatment is encouraging, inadequate
treatment is a serious concern. Emphasis on screening and expansion of treatment
needs to be accompanied by a parallel emphasis on treatment quality improvement.
7,706 citations
TL;DR: Various findings are reviewed in relation to the idea that ACC is a part of a circuit involved in a form of attention that serves to regulate both cognitive and emotional processing, and how the success of this regulation in controlling responses might be correlated with cingulate size.
5,824 citations
"Neural mechanisms of the cognitive ..." refers background in this paper
...Normal inhibitory processing has been associated with activity in the rostral anterior cingulate cortex (ACC...
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TL;DR: In this article, a review examines the role of patient predictors of outcome in cognitive therapy of depression and finds that high pretreatment severity scores are associated with poorer response to cognitive therapy, as are high chronicity, younger age at onset, an increased number of previous episodes, and marital status.
5,556 citations