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Analysis of Brain Mediation and Control of Pain

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Sensitized nociceptors can cause secondary shifts in the central activity processing which causes hyperactivity, making input from the Aβ fibers to be felt as pain. As a result, these patients spontaneously experience pain alongside sensitivity to heat. A similar analysis by Pawl 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 depending 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. Yaksha 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 formation of the arachidonic acid and the stimulation of the nitric oxide synthase (Yaksh, 1999).

As the interneurons are stimulated, the higher order projection neurons via NMDA receptors are also stimulated. This causes an increase in the intracellular calcium, as well as the stimulation of the phospholipase A2 (Yaksh, 1999).  

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