+1 Recommend
1 collections
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Pain and Evil: From Local Nociception to Misery Following Social Harm

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Experiencing pain, especially when chronic, is an excruciating condition that should be regarded as a syndrome, if not a disease. People suffering from chronic pain tend to develop psychological discomfort mostly due to lack of acceptance, disbelief, blame. The complexity of pain pathophysiology, plus a wide range of negative psychosocial factors, leads to a more complex suffering that deserves attention and multidisciplinary treatments. The possibility that chronic pain may occur following physical aggression, torture, or persecution raises the issue of evil as a major contributor to pain in its worst representation – when individuals or groups are attacked based on racial, social, gender, religious, political, or other grounds. To explore the complex issue of chronic pain following physical or psychological harm, and to underscore the need for a multidisciplinary approach to reduce the burden of chronic pain, we discuss the biological mechanisms underlying pain state. We seek to clarify those factors leading to pain chronification, as well as personal and social attitudes that confound patients with chronic pain. The importance of family and social environment is also investigated, as well as personality traits of chronic pain patients that may further hamper successful treatment. The presence of chronic pain, modulated by, for example, acceptance of being a victim of premeditated physical and social violence, makes the issue more difficult to comprehend.

          Related collections

          Most cited references 122

          • Record: found
          • Abstract: found
          • Article: not found

          Empathy for pain involves the affective but not sensory components of pain.

          Our ability to have an experience of another's pain is characteristic of empathy. Using functional imaging, we assessed brain activity while volunteers experienced a painful stimulus and compared it to that elicited when they observed a signal indicating that their loved one--present in the same room--was receiving a similar pain stimulus. Bilateral anterior insula (AI), rostral anterior cingulate cortex (ACC), brainstem, and cerebellum were activated when subjects received pain and also by a signal that a loved one experienced pain. AI and ACC activation correlated with individual empathy scores. Activity in the posterior insula/secondary somatosensory cortex, the sensorimotor cortex (SI/MI), and the caudal ACC was specific to receiving pain. Thus, a neural response in AI and rostral ACC, activated in common for "self" and "other" conditions, suggests that the neural substrate for empathic experience does not involve the entire "pain matrix." We conclude that only that part of the pain network associated with its affective qualities, but not its sensory qualities, mediates empathy.
            • Record: found
            • Abstract: found
            • Article: not found

            Towards a theory of chronic pain.

            In this review, we integrate recent human and animal studies from the viewpoint of chronic pain. First, we briefly review the impact of chronic pain on society and address current pitfalls of its definition and clinical management. Second, we examine pain mechanisms via nociceptive information transmission cephalad and its impact and interaction with the cortex. Third, we present recent discoveries on the active role of the cortex in chronic pain, with findings indicating that the human cortex continuously reorganizes as it lives in chronic pain. We also introduce data emphasizing that distinct chronic pain conditions impact on the cortex in unique patterns. Fourth, animal studies regarding nociceptive transmission, recent evidence for supraspinal reorganization during pain, the necessity of descending modulation for maintenance of neuropathic behavior, and the impact of cortical manipulations on neuropathic pain is also reviewed. We further expound on the notion that chronic pain can be reformulated within the context of learning and memory, and demonstrate the relevance of the idea in the design of novel pharmacotherapies. Lastly, we integrate the human and animal data into a unified working model outlining the mechanism by which acute pain transitions into a chronic state. It incorporates knowledge of underlying brain structures and their reorganization, and also includes specific variations as a function of pain persistence and injury type, thereby providing mechanistic descriptions of several unique chronic pain conditions within a single model.
              • Record: found
              • Abstract: found
              • Article: not found

              Chronic pain-associated depression: antecedent or consequence of chronic pain? A review.

              To determine the current status for the association of chronic pain and depression and to review the evidence for whether depression is an antecedent or consequence of chronic pain (CP). A computer and manual literature review yielded 191 studies that related to the pain-depression association. These reports were reviewed and sorted into seven categories relating to the topic of this paper. Eighty-three studies were then selected according to inclusion criteria and subjected to a structured review. Any medical treatment setting including pain treatment as inclusion criteria for selection of studies. Any patients with any type of chronic pain. The reviewed studies were consistent in indicating that there is a statistical relationship between chronic pain and depression. For the relationship between pain and depression, there was greater support for the consequence and scar hypotheses than the antecedent hypothesis. Depression is more common in chronic pain patients (CPPs) than in healthy controls as a consequence of the presence of CP. At pain onset, predisposition to depression (the scar hypothesis) may increase the likelihood for the development of depression in some CPPS. Because of difficulties in measuring depression in the presence of CP, the reviewed studies should be interpreted with caution.

                Author and article information

                J Pain Res
                J Pain Res
                Journal of Pain Research
                21 May 2020
                : 13
                : 1139-1154
                [1 ]Neurorehabilitation 2, Post-Coma Unit, IRCCS Fondazione Santa Lucia , Rome 00179, Italy
                [2 ]National Health System, Azienda USL Roma 2 , Rome 00157, Italy
                [3 ]Headache Centre, IRCCS Fondazione Santa Lucia , Rome 00179, Italy
                Author notes
                Correspondence: Maria Gabriella Buzzi Neurorehabilitation 2, Post-Coma Unit, IRCCS Fondazione Santa Lucia , Via Ardeatina 306, Rome00142, ItalyTel +39 0651501753Fax +39 0651501752 Email mg.buzzi@hsantalucia.it
                © 2020 D’Ippolito et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                References: 163, Pages: 16
                Expert Opinion

                Anesthesiology & Pain management

                psychological features, pain, evil


                Comment on this article