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      Addressing Evidence Linking Secondary Alexithymia to Aberrant Humor Processing

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          Abstract

          In this review, we explore current literature and assess evidence linking secondary (acquired) alexithymia to aberrant humor processing, in terms of their neurobiological underpinnings. In addition, we suggest a possible common neuropathological substrate between secondary alexithymia and deficits in humor appreciation, by drawing on neurophysiologic and neuroradiological evidence, as well as on a recent and unique single-case study showing the cooccurrence of secondary alexithymia and deficit in humor appreciation. In summary, what emerges from the literature is that the cortical midline structures, in particular the medial prefrontal cortex (mPFC), the anterior cingulate cortex (ACC), and the insular cortex, seem to play a crucial role in the expression of both alexithymia and defective humor processing, while though to a lesser extent, a right hemisphere and bilateral frontoparietal contribution becomes evident. Neurobiological evidence of secondary alexithymia and aberrant humor processing points to the putative role of ACC/mPFC and the insular cortex in representing crucial processing nodes whose damage may produce both the above clinical conditions. We believe that the association of secondary alexithymia and aberrant humor processing, especially humor appreciation deficit, and their correlation with specific brain regions, mainly ACG/mPFC, as emerged from the literature, may be of some heuristic importance. Increased awareness on this topic may be of aid for neurosurgeons when accessing emotion-relevant structures, as well as for neuropsychologists to intensify their efforts to plan evidence-based neurorehabilitative interventions to alleviate the deleterious effects of such interpersonal communication deficits.

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          Most cited references81

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          How do we perceive the pain of others? A window into the neural processes involved in empathy.

          To what extent do we share feelings with others? Neuroimaging investigations of the neural mechanisms involved in the perception of pain in others may cast light on one basic component of human empathy, the interpersonal sharing of affect. In this fMRI study, participants were shown a series of still photographs of hands and feet in situations that are likely to cause pain, and a matched set of control photographs without any painful events. They were asked to assess on-line the level of pain experienced by the person in the photographs. The results demonstrated that perceiving and assessing painful situations in others was associated with significant bilateral changes in activity in several regions notably, the anterior cingulate, the anterior insula, the cerebellum, and to a lesser extent the thalamus. These regions are known to play a significant role in pain processing. Finally, the activity in the anterior cingulate was strongly correlated with the participants' ratings of the others' pain, suggesting that the activity of this brain region is modulated according to subjects' reactivity to the pain of others. Our findings suggest that there is a partial cerebral commonality between perceiving pain in another individual and experiencing it oneself. This study adds to our understanding of the neurological mechanisms implicated in intersubjectivity and human empathy.
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            An Interoceptive Predictive Coding Model of Conscious Presence

            We describe a theoretical model of the neurocognitive mechanisms underlying conscious presence and its disturbances. The model is based on interoceptive prediction error and is informed by predictive models of agency, general models of hierarchical predictive coding and dopaminergic signaling in cortex, the role of the anterior insular cortex (AIC) in interoception and emotion, and cognitive neuroscience evidence from studies of virtual reality and of psychiatric disorders of presence, specifically depersonalization/derealization disorder. The model associates presence with successful suppression by top-down predictions of informative interoceptive signals evoked by autonomic control signals and, indirectly, by visceral responses to afferent sensory signals. The model connects presence to agency by allowing that predicted interoceptive signals will depend on whether afferent sensory signals are determined, by a parallel predictive-coding mechanism, to be self-generated or externally caused. Anatomically, we identify the AIC as the likely locus of key neural comparator mechanisms. Our model integrates a broad range of previously disparate evidence, makes predictions for conjoint manipulations of agency and presence, offers a new view of emotion as interoceptive inference, and represents a step toward a mechanistic account of a fundamental phenomenological property of consciousness.
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              Frontal-subcortical neuronal circuits and clinical neuropsychiatry: an update.

              Frontal-subcortical circuits form the principal network, which mediate motor activity and behavior in humans. Five parallel frontal-subcortical circuits link the specific areas of the frontal cortex to the striatum, basal ganglia and thalamus. These frontal-subcortical circuits originate from the supplementary motor area, frontal eye field, dorsolateral prefrontal region, lateral orbitofrontal region and anterior cingulate portion of the frontal cortex. The open afferent and efferent connections to the frontal-subcortical circuits mediate coordination between functionally similar areas of the brain. Specific chemoarchitecture and multiple neurotransmitter interactions modulate the functional activity of each circuit. Dorsolateral prefrontal circuit lesions cause executive dysfunction, orbitofrontal circuit lesions lead to personality changes characterized by disinhibition and anterior cingulate circuit lesions present with apathy. The neurobiological correlates of neuropsychiatric disorders including depression, obsessive-compulsive disorder, schizophrenia and substance abuse, imply involvement of frontal-subcortical circuits.
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                Author and article information

                Contributors
                Journal
                Behav Neurol
                Behav Neurol
                BN
                Behavioural Neurology
                Hindawi
                0953-4180
                1875-8584
                2019
                18 July 2019
                : 2019
                : 1803624
                Affiliations
                1First Department of Neurosurgery, Medical School, National and Kapodistrian University of Athens, Greece
                2Department of Technologies, Communication and Society, International University of Rome “G. Marconi”, Italy
                3Neuropsychology Section, Departments of Neurology and Psychiatry, University Hospital of Patras and University of Patras Medical School, Greece
                4Department of Speech and Language Therapy, School of Health Sciences, University of Ioannina, Greece
                Author notes

                Academic Editor: Norbert Kovács

                Author information
                https://orcid.org/0000-0002-4474-7566
                https://orcid.org/0000-0002-8137-8253
                https://orcid.org/0000-0002-3216-9025
                https://orcid.org/0000-0001-7495-6863
                https://orcid.org/0000-0002-6498-3929
                Article
                10.1155/2019/1803624
                6668559
                3ddaee9a-8060-41c4-8e5a-80538e09254c
                Copyright © 2019 Panayiotis Patrikelis et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 26 January 2019
                : 9 May 2019
                : 14 May 2019
                Categories
                Review Article

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