CAP does not lend itself to a functional specialization framework of separate 'cognitive' and 'affective' brain regions. Instead, cognitive-affective behaviors are related to networks of brain areas, which are critical for regulating the flow and integration of both cognitive and emotional information. A classic example is the amygdala, which is commonly known as the fear center of the brain. While important for generating the feeling of fear, the amygdala is also integral to cognitive functions such as attention and associative learning. The prefrontal cortex is another region where cognition and emotion are integrated. For instance, activity of cells in the dorsolateral prefrontal cortex have been shown to reflect both working memory and reward expectancy and studies suggest that motivation may be integrated with cognitive information in this region . While neuropsychological assessments emphasize cognitive processes, they often overlook evaluation of cognitive-affective processing as a stand-alone domain, or, as a subprocess within standard domains (e.g., affective-memory, verbal memory, visual memory).
A growing body of research demonstrates alterations in CAPs in neurologically and psychiatric impaired populations. For instance, CAP deficits are widely demonstrable within certain neurodegenerative disorders, including frontotemporal dementia , Parkinson’s , and Huntington’s . In others, CAP appears to be resistant to the decrements found in analogue non-affective domains (e.g., relatively intact affective-memory in Alzheimer's disease) . Systematic negative biases in affective-attention and affective-memory are found in depressed persons. This persists in depression remission and is found in those at heightened risk for depression prior to their first episode . From an etiological perspective, research has demonstrated that sleep disturbance disrupts CAP and has been proposed as a mechanism for initiation and maintenance of mood disorders . CAPs provides a novel framework to understanding onset/maintenance of psychiatric disorders, as well as emotional functioning disturbance following brain insult or neuropathology.
Disturbance of emotion processing in frontotemporal dementia: a synthesis of cognitive and neuroimaging findings . http://www.ncbi.nlm.nih.gov/pubmed/22577002
Accurate processing of emotional information is a critical component of appropriate social interactions and interpersonal relationships. Disturbance of emotion processing is present in frontotemporal dementia (FTD) and is a clinical feature in two of the three subtypes: behavioural-variant FTD and semantic dementia. Emotion processing in progressive nonfluent aphasia, the third FTD subtype, is thought to be mostly preserved, although current evidence is scant. This paper reviews the literature on emotion recognition, reactivity and expression in FTD subtypes, although most studies focus on emotion recognition. The relationship between patterns of emotion processing deficits and patterns of neural atrophy are considered, by integrating evidence from recent neuroimaging studies. The review findings are discussed in the context of three contemporary theories of emotion processing: the limbic system model, the right hemisphere model and a multimodal system of emotion. Results across subtypes of FTD are most consistent with the multimodal system model, and support the presence of somewhat dissociable neural correlates for basic emotions, with strongest evidence for the emotions anger and sadness. Poor emotion processing is evident in all three subtypes, although deficits are more widespread than what would be predicted based on studies in healthy cohorts. Studies that include behavioural and imaging data are limited. Future investigations combining these approaches will help improve the understanding of the neural network underlying emotion processing. Presently, longitudinal investigations of emotion processing in FTD are lacking, and studies investigating emotion processing over time are critical to understand the clinical manifestations of disease progression in FTD.
Ginger, C. (Producer). (2014, February 17). The Cognitive-Emotional Brain [Audio Podcast]. Retrieved from brainsciencepodcast.com. Listen here.
Luiz Pessoa argues that emotion and cognition are deeply intertwined throughout many levels of the brain. The researcher reviews recent discoveries about the amygdala and thalamus that challenge traditional assumptions about what these structures do.
Suchy, Y. (2011). Clinical neuropsychology of emotion. Guilford Press. http://www.amazon.com/Clinical-Neuropsychology-Emotion-Yana-Suchy/dp/1609180720/ref=cm_cr_pr_product_top?ie=UTF8
Pessoa, L. (2008). On the relationship between emotion and cognition. Nature Reviews Neuroscience, 9(2), 148-158. http://www.nature.com/nrn/journal/v9/n2/full/nrn2317.html
Boller, F., El Massioui, F., Devouche, E., Traykov, L., Pomati, S., & Starkstein, S. E. (2002). Processing emotional information in Alzheimer's disease: effects on memory performance and neurophysiological correlates. Dementia and Geriatric Cognitive Disorders, 14(2), 104-112. http://www.ncbi.nlm.nih.gov/pubmed/12145458
 LaBar, K. S., & Cabeza, R. (2006). Cognitive neuroscience of emotional memory. Nature Reviews Neuroscience, 7(1), 54-64. http://www.ncbi.nlm.nih.gov/pubmed/16371950
 Pessoa, L. (2008). On the relationship between emotion and cognition. Nature Reviews Neuroscience, 9(2), 148-158. http://www.nature.com/nrn/journal/v9/n2/full/nrn2317.html
 Kumfor, F., & Piguet, O. (2012). Disturbance of emotion processing in frontotemporal dementia: a synthesis of cognitive and neuroimaging findings. Neuropsychology review, 22(3), 280-297. http://www.ncbi.nlm.nih.gov/pubmed/22577002
 Ariatti, A., Benuzzi, F., & Nichelli, P. (2008). Recognition of emotions from visual and prosodic cues in Parkinson’s disease. Neurological Sciences, 29(4), 219-227. http://www.ncbi.nlm.nih.gov/pubmed/18810595
 Hennenlotter, A., Schroeder, U., Erhard, P., Haslinger, B., Stahl, R., Weindl, A., ... & Ceballos‐Baumann, A. O. (2004). Neural correlates associated with impaired disgust processing in pre‐symptomatic Huntington’s disease. Brain, 127(6), 1446-1453. http://www.ncbi.nlm.nih.gov/pubmed/15090475
 Boller, F., El Massioui, F., Devouche, E., Traykov, L., Pomati, S., & Starkstein, S. E. (2002). Processing emotional information in Alzheimer's disease: effects on memory performance and neurophysiological correlates. Dementia and Geriatric Cognitive Disorders, 14(2), 104-112. http://www.ncbi.nlm.nih.gov/pubmed/12145458
 Leppänen, J. M. (2006). Emotional information processing in mood disorders: a review of behavioral and neuroimaging findings. Current opinion in psychiatry, 19(1), 34-39. http://www.ncbi.nlm.nih.gov/pubmed/16612176
 Walker, M. P., & van Der Helm, E. (2009). Overnight therapy? The role of sleep in emotional brain processing. Psychological bulletin, 135(5), 731. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2890316/