Chronic pain is one of the most significant medical and scientific challenges in western society today. As well as the emotional and physical effects on the individual it proves to be a significant financial burden to society. Studies have shown that chronic pain leads to central sensitisation that is partially regulated by release of proinflammatory molecules within the CNS. Most work has concentrated on the role of the spinal cord and little is known about changes in supraspinal regions. The CFA footpad model was used to investigate the expression of inflammatory mediators in the brain in persistent inflammatory pain. Using RT-PCR, gene expression of inflammatory mediators was measured in various brain regions. Consistent with previous reports at 7 and 14 days post-injection IL1β expression was significantly elevated in the posterior of the brain (p<0.05), TNFα showed differential expression with a significant increase in the posterior ipsilateral brain region at 72 hours (p<0.05). The chemokine CXCL1 was significantly elevated at 6 hours post-injection (p<0.05) suggesting a role for this chemokine in regulation of the acute pain response. Contrary to evidence from the spinal cord, CX3CL1 and its receptor CX3CR1 were down regulated in the brain at 6 and 24 hours post-injection. Differential expression of astrocyte activation was identified by GFAP immunochemistry. Hypoxia has been implicated in neurodegeneration, a process thought to play a role in chronic pain. Here Hypoxia inducible factor (Hif1α) mRNA expression within the brain was not altered in a CFA model of peripheral inflammation. Interestingly, using Hypoxyprobe immunohistochemistry, a higher level of hypoxia was identified in non-injected controls than in CFA treated animals. This is the first evidence of differential chemokine expression in the brain in persistent inflammatory pain and the first study to suggest a potential role for differential oxygenation within the brain in this condition.

Phantoms in the Brain

Studies on chronic pain mechanisms in the central nervous system

Spiritual Development in Children and Adolescents

This chapter discusses emotions as the affective markers of experience. The bridge for social interactions is built by emotions which play the role of narrators of physical, mental, and social health for oneself and for others. When from one point of view emotions guide neural mechanisms for physiological and chemical balance, from another viewpoint emotion enhances self-expression and the presentation of the person. The study of emotion bring in the role of the brain, the body, and the self, interspersed by the influence of environment, society, art, and one’s character. In this chapter that focus on emotions I discuss the following questions: Why and for what outcome does the brain generate emotions? How are feelings and emotions different? Are feelings always dependent on sensations? Are there feelings that are not dependent on sensations? Can feelings be considered as discrete cognitive events and understood within the framework of neuroscience? Another pertinent issue that is discussed currently is the ability of emotions to be part of a decision-making process by contributing to the cognitive deciders. Do emotions influence our cognitive capacities and rational processes?

The Feel Factor: Qualia and the Affective Markers of Experience

This paper provides a brief chronicle of medicine and narratives, the aim being to understand the role of people's narratives historically, including how they have developed and changed over time, and in particular the rising interest in the neuro‐narrative. The paper ends by reflecting on what practicing physicians, nurses, therapists, and social care workers might want to think about when considering the use of narratives with their clients.

Medicine and patient narratives

PHILIP GERRANS “A One-stage Explanation of the Cotard Delusion” provides an elegant example of the application of neuroscientific findings to known clinical phenomena in psychiatry. Gerrans argues that, in the cases of the Cotard and Capgras delusions, a one-stage explanation is sufficient to account for the clinical phenomena. That is, the neuroanatomic defect and the consequent anomalous experience are sufficient to produce the delusion. According to Gerrans, we do not need to postulate that the delusion will emerge only if the anomalous experience is filtered through a faulty reasoning process (a two-stage explanation). Against the argument of Young and Leafhead (1996) that Cotard and Capgras delusions stem from the same neuroanatomic deficit and differentiate only in being processed differently—thus requiring a two-stage explanation—Gerrans argues that the respective neuroanatomic defects are in fact different, and that, therefore, the two delusional syndromes differ at the first stage and do not require the two-stage explanation suggested by Young and Leafhead. I do not have an opinion as to who is right in this disagreement, and I will devote these remarks to explaining why I do not have an opinion. In developing this explanation I will touch on what I find problematic in many discussions of neuroscience, neurocognitive models, and clinical psychiatry; I will thus use this article to highlight those problems. On the face of it, one would think that the issue raised by Gerrans should admit of a simple resolution. He argues that Capgras and Cotard delusions derive from different neural defects. Young and Leafhead, on the other hand, base their two-stage argument on the argument that the two delusions derive from the same neural defect. So which is it? Neuroscientists should be able to settle the issue and end the dispute. Gerrans remarks “that we need to look more closely at the CN [cognitive neuropsychiatric] explanation of the Capgras delusion.” As he describes it, face recognition involves two components, a cognitive and an affective component, with separate neuroanatomic substrates. An individual successfully recognizes the face of a friend or acquaintance when she matches the cognitive recognition (cognitive component) with the affective tone of familiarity (second component). When there is a lesion in the neural substrate of the affective component, she may recognize the face but without the tone of familiarity. In her effort to understand her affective experience of the face as alien rather than as familiar, she may conclude that her friend has been replaced by a double. Thus we have the Capgras delusion. Let us now unpack this explanation. According to Gerrans, researchers have hypothesized

https://muse.jhu.edu/journals/philosophy_psychiatry_and_psychology/v009/9.1phillips.pdf

Phantoms in the Brain

Citations

Studies on chronic pain mechanisms in the central nervous system

Spiritual Development in Children and Adolescents

The Feel Factor: Qualia and the Affective Markers of Experience

Medicine and patient narratives

Arguing From Neuroscience in Psychiatry

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