How the Brain Mediates and Controls the Sensation of Pain Term Paper

How the Brain Mediates and Controls the Sensation of Pain - Term Paper Example Now, with the advent of Magnetic Resonance Imaging, and other non-invasive assessment technologies, the less invasive, but more direct and accurate examination of the brain has been made possible. The areas of the brain which now respond and which manage pain perception and sensation can now be laid out and understood by practitioners. The more technical processes of pain sensation and mediation can now be assessed and evaluated. It is popular knowledge that the brain controls and manages all types of sensation and feelings in our body. Understanding the more specific patterns which explain these control functions in the brain are more complicated and need a more thorough analysis. This study shall now seek to discuss how the brain mediates and controls the sensation of pain. It shall first present an anatomical discussion of pain sensation, and then a deeper analysis of brain mediation and control of pain shall be carried out. An emphasis on the central mechanisms of pain and the bi ological and neurochemical processes underlying them shall be presented in this paper. This study is being undertaken with the purpose of establishing a clear and comprehensive understanding of the brain functions as it mediates and controls pain sensations. ... In effect, sensitized nociceptors can cause secondary shifts in the central activity processing which causes hyperactivity, making input from the A? fibers to be felt as pain (Baron, 2000). As a result, these patients spontaneously experience pain alongside sensitivity to heat. A similar analysis by Pawl (1999) discussed pain as assessed by the brain through function images. In his analysis, he was able to confirm that during the pain experience, increased activity in the sensory pathways from the thalamus to the sensorimotor cortex was apparent. Pawl (1999) also established that the contralateral hippocampus became active during experimental heat pain; during acute pain, activity in the amygdala was also increased. In studies covering chronic pain, the nociceptive disruptions often activated the same areas; but these same areas were manifestly less active in instances of pain which originated psychogenically (Pawl, 1999). This analysis implies the more apparent pathways for pain dep ending on the kind and the source of pain. Based on the analysis by Yaksh (1999), the regulation of afferent processing is at the level of the spine. Yaksh analysis is more detailed in terms of the involvement of the NMDA and the NKI receptors. Aside from systems which can reduce excitability, the post-tissue injury pain condition is marked by the upregulation of gain. As a result, continuous small afferent excitation triggers a cascade which is instigated by the release of amino acids and peptides. With the activation of the NMDA and NKI receptors, there is a rise in intracellular calcium and the stimulation of the kinases and the phospholipase A2 (Yaksh, 1999). The NMDA then acts as the phosphorylate membrane channels and receptors; while the NKI causes the