Abstract
We have reviewed here the neuroanatomical and neuropsychological literature of the human brain and have proposed the various pain mechanisms that we currently know of. Essentially when tissue is damaged, peripheral nociceptors are activated continuously and prostanoids are hence produced. Nonsteroidal anti-inflammatory drugs (NSAIDs) and medications aim to target these prostanoids to treat the inflammatory component of pain. Normal pain tends to have a protective response. It is important for the nervous system to learn and recognize this painful stimulus earlier and quicker with repeated exposure to avoid tissue damage. This neuronal plasticity and gain in sensitivity result in sensitization of the nervous system, both centrally and peripherally and help in earlier detection of the pain sensation. However, persistent pain can become pathologic and will eventually result in the loss of protection pain offers to the body. Pain-related fear has been implicated in the transition from acute to chronic low back pain and the persistence of disabling low back pain, making it a key target for physiotherapy intervention. The current understanding of pain-related fear is that it is a psychopathological problem where people who catastrophise about the meaning of pain become trapped in a vicious cycle of avoidance behaviour, pain and disability, as recognised in the fear-avoidance model. We looked at how pain is perceived, especially in low-back pain patients. It has been hypothesized that individuals with low-back pain (LBP) can change their motor behavior, which is fundamentally an adaptation mechanism aimed at minimizing the real or perceived risk of further pain.
Highlights
BackgroundAcute and chronic pain puts a significant clinical, economic, and social burden on humanity [1]
We looked at how pain is perceived, especially in low-back pain patients
The Institute of Medicine (IOM) states that more than a 100 million Americans suffer from chronic pain [2]
Summary
Acute and chronic pain puts a significant clinical, economic, and social burden on humanity [1]. This, in turn, activates nociceptive neurons in the spinal cord and can release glutamate, which further triggers the neurons and can make the N-methyl-D-aspartate (NMDA) receptors more sensitive to glutamate in a process called “central sensitization” [6] Before this sensitization, the information from activated nociceptor fibers is relayed to the spinal cord by the sensory cells located in the dorsal root ganglia. These interact with the afferent fibers, interneurons, and projection neurons of the dorsal horn Actions at these sites either suppress or enhance passage of nociceptive information to the periaqueductal gray, nucleus tractus solitarus, amygdala and other structures involved in secondary processing. Opioids act via presynaptic and postsynaptic inhibitory effects on central and peripheral C-fiber terminals, spinal neurons, and supraspinal mechanisms targeting the descending pain modulatory system [11] This is most notable in the periaqueductal gray, an area highly involved in processing placebo analgesia [39]. Still much remains to be discovered about the many functions of the brain in the processing of pain, and new evidence from functional neuroimaging and clinical neuropsychology is affording new insights of the human cortex [40]
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