To attain a greater depth of understanding into the cognitive processes - that govern all emotional-based decision making and mental expression - an insight into the neuroanatomical aspects of an affecting mental state can help affirm the underlying mechanisms of a mental health disorder, such as: depression. In terms of diagnosis, great progress into the detailing of neurological mechanisms and structures have been possible due to the introduction of improved neuroimaging methods; where before diagnosis and the study of mental health was reliant primarily on patient behavioural assessments [1]. Such advancements have enabled the growth of disciplines built on top of cognitive sciences, like: Affective Neuroscience, which is the study of neural mechanisms involved in emotion and mood generation, and has been promoted by the works of Davidson et al. where they have described the primary brain regions involved in depression as: the prefrontal cortex (PFC), anterior cingulate cortex (ACC), hippocampus, and the amygdala; however, it is difficult to limit the specificity of neurological deterioration to abnormality in single regions of the brain, and rather the cause of mental disorder is most likely from the malformation of complex interrelating neural circuitry, that forms the structural networks governing cognitive processes [2, 6, 1].
It has been stated that the cortical-subcortical circuit – for which the PFC regions are a constituent of – is the most prevalent circuitry that ubiquitously demonstrates reductions in brain matter and abnormal cognitive functionality across patients suffering from depression [1, 2, 3, 4, 5, 6]. Some of the core responsibilities of PFC regions in neural mechanics is in the management of emotional-based decision making and the regulation of regions involved in emotion generation and processing; moreover, a key aspect of patients suffering from depression is their persevering negative feelings that negate their motivation to achieve goals, which is probably due to the associating deficiency in their PFC regions, that are supposed to regulate emotive polarity and produce positive anticipatory signals that incentivise and guide goal-orientated behaviours, such as: satisfying appetite [2, 1, 4, 7].
In consequence, for some types of depression, the cognitive deficit in anatomical projections – from the PFC regions – required for regulatory functionality, can result in the lack of inhibitory mechanisms towards the amygdala region; effectively increasing the possibility of persistent amygdala hyperactivity, which is an integral neural component for generating emotion most relevant to aversive respondence [4, 2]. Aversive respondence involving an individual’s ability to both interpret and emotionally process perceptual stimuli that signals environmental uncertainty and threats, effectively inducing negative feelings, such as: anxiety and fear. A similar maladaptive emotional response that incorporates the persistence of negative feeling is the dysregulation – leading to hyperactivity – of the hippocampus – which is responsible for the processing of stimuli in respect to context – effectively contributing to an individual’s abnormally persistent emotional response to unsettling stimuli even when the contextual causation has subsided, for instance: severe mourning over a hyperextended period of time [1, 2].
Another key neurological constituent of the abnormal neural circuitry inducing and prolonging depression is the ACC, which is critical in the management of conflicting cognitive instances that involve the evaluation of received stimuli in relevance to an individual’s current internal state, for instance: the attentive effort of overcoming a threatful adversary forcing decisive adaption; therefore, providing the regulatory pathways between cognitive respondents, such as: the PFC and amygdala, required for realised stresses and the corresponding emotive-based expressions [2]. In cases of depression, without inhibition, the ACC can be found increased in activity causing the anatomical projections of persistent re-experiencing of negative feelings that originate from a hyperactivate amygdala that has not been inhibited by an effective PFC, rather than lessening the magnitude of negative feelings overtime through healthy reappraisal [4, 5, 6, 7]. In physical states of emotional regulatory dysfunction, it is this integral connectivity between the PFC, ACC, and amygdala that contributes to the onset of depression, as well as, persistence of emotional negativity.
In effect, with regards to cognitive processes, the detailed neuroanatomical aspects of mental health disorders, and their corresponding mechanisms, demonstrate the somewhat preconditioned influences guiding behavioural expression. Expressions of a mental capacity limited by the attributive state of functionality and physical neurological integrity existing for a given individual; therefore, too some degree, offering – where outward behavioural coping mechanisms have been unsuccessful – a validity in the concept that mental expressions, as well as, physical behavioural expressions, are indeed without doubt motivated by the aggregate mental state of dysfunctional cognitive processes and mechanisms that exist from an abnormal, diseased, maladaptive neuroanatomical state.
[ 1 ] Zhang, F. F., Peng, W., Sweeney, J. A., Jia, Z. Y., & Gong, Q. Y. (2018) Brain structure alterations in depression: Psychoradiological evidence. CNS neuroscience & therapeutics, vol 24 (11) pp. 994–1003. DOI: 10.1111/cns.12835
[ 2 ] Davidson, R. J., Pizzagalli, D., Nitschke, J. B., & Putnam, K. (2002) Depression: Perspectives from Affective Neuroscience. Annual Review of Psychology, vol 53 pp. 545-574. DOI: 10.1146/annurev.psych.53.100901.135148
[ 3 ] Cotter, D., Mackay, D., Chana, G., Beasley, C., Landau, S., & Everall, I, P. (2002) Reduced neuronal size and glial cell density in area 9 of the dorsolateral prefrontal cortex in subjects with major depressive disorder. Cereb Cortex, vol 12 (4) pp. 386-94. DOI: 10.1093/cercor/12.4.386
[ 4 ] Lu, Q., Li, H., Luo, G., Wang, Y., Tang, H., Han, L., & Yao, Z. (2012) Impaired prefrontal-amygdala effective connectivity is responsible for the dysfunction of emotion process in major depressive disorder: A dynamic casual modelling study on MEG. Neuroscience Letters, vol 523 (2) pp. 125-130. DOI: 10.1016/j.neulet.2012.06.058
[ 5 ] Johnstone, T., van Reekum, C. M., Urry, H. L., Kalin, N. H., & Davidson, R. J. (2007) Failure to regulate: counterproductive recruitment of top-down prefrontal-subcortical circuitry in major depression. The Journal of neuroscience : the official journal of the Society for Neuroscience, vol 27 (33) pp. 8877–8884. DOI: 10.1523/JNEUROSCI.2063-07.2007
[ 6 ] Erk. S., Mischl, A., Stier, S., Ciaramidaro. A., Gapp, V., Weber, B., & Walter, H. (2010) Acute and Sustained Effects of Cognitive Emotion Regulation in Major Depression. Journal of Neuroscience, vol 30 (47) pp. 15726-15734. DOI: 10.1523/JNEUROSCI.1856-10.2010
[ 7 ] Beauregard, M., Paquette, V., & Lévesque, J. (2006) Dysfunction in the neural circuitry of emotional self-regulation in major depressive disorder. Neuroreport, vol 17 (8) pp. 843-846. DOI: 10.1097/01.wnr.0000220132.32091.9f