Neural mechanisms of emotions, alexithymia, and depression

This chapter brings the powerful conceptual tools of the science of parallel distributed processing (PDP) to bear on the cognitive neuroscience of emotions discussed in this book. Cerebral representations are encoded as patterns of activity involving billions of neurons. PDP across these neuronal populations provides the basis for a number of emergent properties: (1) processing occurs and knowledge (long term memories) is stored (as synaptic connection strengths) in exactly the same networks; (2) networks have the capacity for setting into stable attractor states corresponding to concepts, symbols, implicit rules, or data transformations; (3) networks provide the scaffold for the acquisition of knowledge, but knowledge is acquired through experience; (4) PDP networks are adept at incorporating the statistical regularities of experience as well as frequency and age of acquisition effects; (5) networks enable content-addressable memory; (6) because knowledge is distributed throughout networks, they exhibit the property of graceful degradation; (7) networks intrinsically provide the capacity for inference. With this perspective, I propose a new model of emotional function that reasonably accounts for the effects of focal lesions at various points (insula, orbitofrontal cortex, convexity cortex, and intervening white matter) due to stroke, trauma, surgery, and degenerative disease, as reflected in disorders of affective prosody, facial emotional comprehension and expression, emotional behavior, and personality. I consider a modification of the James Lange theory that takes into account the role of a lifetime of subjective knowledge acquisition by the orbitofrontal cortex. Alexithymia is conceptualized as a disorder of the insula/orbitofrontal cortex/dorsolateral prefrontal cortex (DL-PFC) system, the function of which can be disrupted by degradation of knowledge at a number of different locations. Finally, I consider the possibility that depression reflects pathological learning involving the medial and lateral orbitofrontal cortices such that there is a pathologic engagement of the two regions, as suggested by Rolls. I conclude with a consideration of the peculiar responsivity of depression to serotonergic and noradrenergic agents, as well as to surgical orbitofrontal undercutting, and what that might be telling us about the mechanisms of depression and its treatment.