Summary of Principles of Cognitive Neuroscience by Purves a.o. - 2nd edition
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Summary with the article: What has neuroscience ever done for us? - Roiser (2015). focusing on the role of neuroscience in psychological research
Despite the developments in neuroscience over the past 25 years, the standard treatments of mental health problems hardly changed. In this article it will be described why there exists such a disconnect between knowledge and application and could we increase the effectiveness of existing treatments and developing new treatments?
Although there is strong evidence that pharmacological and psychological interventions can be effective in treating depression, there are still many people who suffer from depression and die from suicide. The costs of mental health problems are very high but why do they remain so high despite treatment has improved? It is a great challenge to choose the right treatment for the right individual. There is large variability in the effectiveness of treatments for different people. In a study of Trivedi and colleagues (2006), only one third of the participants with a depression recovered fully after antidepressant prescription and Cuipers and colleagues (2014) found that less than half recovered fully across various kinds of psychotherapies of which cognitive behavioural therapy performed the best.
The only positive influence of neuroscience research on mental health practice has been the use of animal models to develop new drugs, which has resulted in a few new treatments over the past ten years. The difference between neuroscience and mental health reflects the problem of consciousness: How does the brain generate experience? Linking neurons to experience is still a huge challenge. Measurements can be related to behaviour but experience can only be inferred indirectly. Mental health practice takes subjective experience as its starting point, there is no objective test for it. Practitioners rely on descriptive definitions in which the symptoms specify the spectrum of diagnosis.
Mapping symptomatically and categorically defined mental disorders onto brain circuits is an impossible task because individuals diagnosed both with depression can have different combinations of symptoms and therefore these presentations do not necessarily correspond to one underlying causal mechanism. Also, the same symptoms could be caused by different mechanisms. The difference with conditions such as a coughing, is that this is defined mechanistically and not according to symptoms. This example illustrates the limitations of a symptom-based diagnostic system when selecting a treatment. One single mechanism for depression is not possible and therefore depression cannot be diagnosed with a brain scan. Neuroscientific measurements are more appropriate in spectrum approaches than in categorical models which is one of the reasons that the American National Institute of mental health decreased the funding of studies based on descriptive categorical diagnoses. An experienced therapist might be able to adjust an intervention according to identified underlying factors but there is still a lot of trial and error in treatment selection.
According to the author it is needed to specify symptoms at brain level. It might be argued that in this way the psychosocial contexts is ignored but brain function is influenced by both genetics and social environment. Brain-based explanations of symptoms should include both biological and psychosocial explanations. These are different levels of the same question and therefore integration of both frameworks is required.
Symptoms can be lying on a spectrum with proximal on the one side and distal at the other side. Proximal causes are directly related to mechanisms causing symptoms and are targets for treatment. These are identified by fundamental research. Distal causes are indirectly related to the mechanisms causing symptoms and are targets for prevention. These are identified through epidemiological research. More knowledge about proximal causes, might contribute to better treatment.
Research on depression has focused on distal (underlying) causes such as heritability, genetics, life experience and personality. Proximal causes include: various forms of stress, psychological constructs such as dysfunctional negative schemata, information processing biases and disrupted transmission in neurotransmitter systems. These factors are not specified at the level of activity in the brain circuits. There is also no strong evidence for the serotonin hypothesis, that low levels of this hormone directly elicit depressive symptoms. It is tried to specify depression at the level of brain circuits. Several studies suggest that negative affective perception and experience in depressed people are caused (proximally) by disrupted function in the brain circuits that support normal emotional processing. There are robust abnormalities found in the subgenual anterior cingulate cortex (sgACC) during emotional processing (The sgACC was reduced in volume).
It can be concluded that ‘depression’ does not have one mechanism and that it is not a single entity at brain level. Despite statistical evidence at group level for the reduced volume of the ssACC, this cannot be identified at an individual level. Will we be able to exploit this variability in brain structure and function among individuals with the same diagnosis to improve treatment choice? Several studies are conducted on emotional processing in individuals with depressive symptoms. The results show that psychological treatment was the most effective in individuals with normal baseline sgACC activation during negative emotional processing and pharmacological treatments were better if the baseline activation of the sgACC was abnormal. The identification of these abnormally functioning regions resulted in both invasive and non-invasive methods, such as deep brain stimulation (DBS). Interesting preliminary results found in research on DBS have to be replicated in randomised controlled trials. Non-invasive methods such repetitive transcranial magnetic stimulation (rTMS) has already been approved in America. Recently, a new method in which visuo-spatial distraction is used to prevent the consolidation of memories after a traumatic experience has been developed.
Although neuroscience has not had a large impact on mental health practice yet, an interesting period is coming. In the short term we should change the way we think about symptoms, focusing on proximal causes at brain level and how these relate to psychological processes. By accepting a mechanistic variety, an improved classification systems and new approaches and tools should be developed in order to improve the treatment selection for the individual.
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