Sensitization refers to a phenomenon in which parts of the nervous system that communicate pain information become too sensitive and therefore more likely to send exaggerated pain signals when stimulated. Within the spinal cord, after repeated activation of the nociceptors, the WDR neurons described earlier take on a higher degree of readiness and become more sensitive to incoming stimuli (Ji, et al., 2018). These cells become more excitable and more receptive to incoming information. Also, in chronic pain, incoming nerves that terminate in the spinal cord begin to sprout new connections. As a result, pain thresholds are reduced (hyperalgesia) and even non-painful stimulation (allodynia) of the affected body part may be perceived as painful(Ji, et.al, 2018; Institute for Chronic Pain, 2017). This process is actually normal, and typically these cells will return to their pre-pain levels when tissue damage has healed and incoming painful signals have ceased (Institute for Chronic Pain, 2017). However, in persons with chronic pain, the newly sensitized neurons do not appear to return to normal, and instead remain oversensitive to stimulation and pain (Ashmawi and Freire, 2016). See Text Box 2 for a useful analogy when explaining the sensitization model to patients with chronic pain. It is unclear why some individuals are more prone to lasting sensitization than others, although there is some evidence that genetics plays a significant role (Ingraham, 2020; Institute for Chronic Pain, 2017). Sensitization to pain also appears to take place in the brain itself, where pain is processed and interpreted. As described above, there are many complex and interconnected brain structures involved in processing pain signals. These structures are called the pain neuromatrix . Evidence suggests that chronic pain leads to lasting alterations in the structure, functionality, and neurochemistry of this neuromatrix and a decrease of nociceptive pain and non-nociceptive mechanisms is required to produce the perception of pain (Trachsel and Cascella, 2020; American Posture Institute, 2017). Like the changes in sensitization at the spinal level, these changes mean that one becomes more sensitive to pain and may experience pain from stimuli that are usually not painful. Endogenous chemicals released from the sites of tissue injury can sensitize both the peripheral neurons and neurons within the central nervous system which can result in allodynia and hyperalgesia. Further, sensitization can involve a heightened response to nociceptive (pain) stimuli, in which membrane excitability and synaptic transmission of nociceptive signals are increased and there is a decreased inhibitory effect of nociceptive stimuli in the dorsal horn neurons (Ashmawi and Freire, 2016; Wei, et al., 2019). Furthermore, many brain regions are designed to inhibit or control other brain regions, and evidence exists that overuse resulting from chronic pain may lead to imbalances between brain structures. For example, a region of the brain called the dorsolateral prefrontal cortex is believed to inhibit the functioning of two other regions – the medial and orbitofrontal cortices. When an individual experiences pain, the medial and orbitofrontal regions are believed to generate suffering and feelings that the pain is unpleasant. How long that feeling lasts is determined in part by the dorsolateral prefrontal cortex, which kicks in to decrease or manage the suffering element of pain. If the medial and orbitofrontal regions are the “accelerator” in pain, the dorsolateral prefrontal cortex serves as the “brakes.” However, several studies of chronic pain have shown that, in people with chronic pain, the dorsolateral prefrontal cortex is slightly atrophied – meaning that there may be less capacity for “braking” the emotional reaction – possibly resulting in a more severe and long-lasting negative emotional response to pain (Yang and Chang, 2019).
Rather than seeking a definition that differentiates acute pain from chronic pain, it may be better for clinical purposes to think of each term according to its basic characteristics described below. Acute pain Acute pain refers to pain elicited by the injury of bodily tissues and/or the activation of nociceptors. In general, acute pain lasts for a limited amount of time and remits when the underlying pathology resolves. Acute pain is a frequent reason for seeking treatment from healthcare providers and occurs after trauma (including injuries and burns), after surgical interventions, in acute headache, or as a part of a disease process such as dental decay. A pulpitis is a good example of a condition that produces acute pain. Chronic pain Chronic pain is usually initiated by an injury, but is perpetuated by factors that are largely unrelated to the original injury. Chronic pain extends over long periods of time and does not usually represent ongoing tissue damage. In many cases, chronic pain is not directly related to an underlying medical pathology that can explain it. That does not mean that chronic pain isn’t “real”; it just means that there is rarely a simple anatomical explanation for chronic pain that can be easily identified or detected with medical tests. However, there are certainly situations, such as osteoarthritis or nerve damage in the face secondary to trauma, in which a persistent medical condition can result in chronic pain. It is important to keep in mind that many individuals with chronic pain may also experience intermittent acute pain. For example, an individual with chronic pain from osteoarthritis of the temporomandibular joint might experience a flare-up in joint Although the pain model described above makes sense for immediately painful experiences, it does little to explain why pain sometimes persists or becomes chronic. Initially, a painful injury results in signals being sent to the central nervous system and eventually being interpreted as pain. Furthermore, when inflammation or a disease process exists, the signal for pain is constantly being sent to the brain along the routes described above. But what happens when the wound heals and the swelling goes down? Why is there still a pain signal? And even when there is chronic irritation of a nerve, and therefore a good reason for pain, why is pain more disabling for some than for others? Understanding factors that lead acute pain to become chronic pain, and those that contribute to pain-related disability, has been the focus of considerable research over the past 50 years. Studies have identified both biological and psychosocial factors that help to explain this phenomenon. Biological factors include sensitization of nerves and changes in the brain; psychosocial factors include a number of behavioral, cognitive, and social elements that seem to prolong the pain experience. Biological factors For many years, it was believed that chronic pain was essentially a psychological phenomenon, in which “vulnerable” individuals maintained pain symptoms as a way to express anxiety, to get needed reassurance, or to maintain the “sick role”; however, although psychological features are certainly important in chronic pain (and are discussed in more detail later in this course), more and more evidence indicates that the central nervous system actually seems to change in response to long- term painful stimulation, and that these changes may also underlie chronic pain (Yang and Chang, 2019). Long-term changes mean that individuals with chronic pain may develop an abnormal regulation of pain signals in the central nervous system itself. This is referred to as the sensitization model of chronic pain. pain after a long dental appointment. Why does acute pain become chronic?
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