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3 What are the major types of pain?

The best approach to understanding and designing effective treatment plans for pain is to view the origins of the problem in terms of basic pain mechanism. This is because the pain mechanism has a major impact on: (i) the potential to diagnose a specific condition, (ii) choose an effective treatment, (iii) prognosticate the patient's course in therapy, and (iv) guide the patient in self‐management. There are three major mechanism‐based types of pain: nociceptive, inflammatory, and neuropathic (Figures 3.1 and 3.2).

Figure 3.1 The basic mechanisms of pain.

Figure 3.2 How basic pain mechanisms interact.

Nociceptive pain is pain arising from acute injury. It is signaled by the normal functioning of the nociceptive processing system (Chapter 2). Primary afferents in the various parts of the body are activated by peripheral signaling molecules or direct energy transfer. Currently we know that all of the body is innervated by afferents with some exceptions: the nucleus pulposus of the vertebral disc, the brain parenchyma, and cartilage. Signaling molecules involved in nociception include: protons, bradykinin, histamine, acetylcholine and others (Ringkamp et al. 2013). Direct energy transfer can occur from pressure‐type stimuli, thermal stimuli (hot and cold), or electric shock. A specific nociceptive stimulus may be sensed by multiple primary afferents, as there is no one afferent that is exclusively responsible for pain. Thermal stimuli are sensed by multiple fiber types, for example when touching a hot stove, there is “first pain” that provokes an immediate withdrawal response, mediated by Aδ fibers, and “second pain” mediated by C fibers that behaviorally reinforce avoidance of damaging stimuli. Nociceptive pain intensity is highly variable depending on personal and contextual factors. Nociceptive pain can be highly responsive to treatments; ideal treatment varies with the intensity, focality, and cause of the pain. In general, mild‐to‐moderate nociceptive pain responds well to over‐the‐counter analgesics, e.g. NSAIDs, acetaminophen; severe nociceptive pain may require opioids or special management strategies such as nerve blocks. Nociceptive pain has a good prognosis, but evidence indicates that very strong nociceptive stimuli may predispose patients to chronic pain.

Inflammatory pain is established by exposure to inflammatory signaling molecules and includes pain in response to normally non‐painful stimuli. A classic example of this is osteoarthritis: at first, normal walking activity is uncomfortable; later with continued disease, unbearable. Common examples include sunburn, in which light touch fibers are recruited to signal pain making a bag strap intolerable, and ingrown toenails which can make the pressure of a comfortable shoe excruciating. In inflammatory pain, the primary afferents in the body undergo sensitization by inflammatory signaling molecules, including: Nerve Growth Factor (NGF), Tumor Necrosis Factor‐alpha (TNFα) Interleukin 6 (IL6), bradykinin, protons, and other substances (Ringkamp et al. 2013). The sensitization of the nerve endings results in long‐lasting changes in afferent signaling, termed “phenotypic switching.” Potentially reversible, the phenotypic switch means that the afferents formerly responsible for nonpainful sensations now signal pain. This is how the pressure of a bag strap or shoe becomes uncomfortable once inflammatory pain signaling is activated. If peripheral inflammation resolves, this increased pain signaling may be reversible. In other situations, such as osteoarthritis, inflammation persists and the pain continues. Inflammatory pain may respond to NSAIDs or corticosteroids, however it is also important to address the origins of inflammatory pain. Specific “disease‐modifying” therapies include physical therapy, disease‐modifying drugs, ergonomic adaptations, or surgery.

Neuropathic pain arises from disease, damage, or dysfunction of the nervous system. There are many nervous system conditions manifesting pain including multiple sclerosis, post‐herpetic neuralgia, myelopathy, nerve root compression, and peripheral neuropathy. In these cases, pain is driven by abnormal signaling arising from the pain‐sensing system itself (Devor 2013). This pain can be difficult to treat if the underlying abnormality is not rectifiable. Neuropathic pain is not highly responsive to NSAIDs, and generally prescription medications are required. Multiple treatment options are available. Pain‐active anticonvulsants such as gabapentin or pregabalin, or pain‐active anti‐depressants, such as amitriptyline or duloxetine can provide relief, Chapter 19. Although these neuromodulating medications are not universally effective, substantial pain relief may follow when careful attention is applied to titrating medication and addressing the underlying condition. In neuropathic pain, disease modifying therapies are especially valuable. Some forms of neuropathic pain are treatment resistant.

The presence of abnormal pain responses during clinical examination aid in distinguishing nociceptive, inflammatory, and neuropathic pain. Abnormal pain signaling is recognized by the presence of allodynia or hyperalgesia. To explain these terms, it's necessary to introduce the stimulus‐response curve. Pain is systematically assessed in clinical and pre‐clinical trials using a stimulus response curve, this is a graph that represents a person's rating of sensory intensity (pain) in response to a certain stimulus (Figure 3.3). Imagine touching a metal surface of a certain temperature. At room temperature, there is no pain. As the temperature rises, at some point there is a twinge of pain, this is the pain threshold. As temperature increases further, pain ratings increase, usually forming an S‐shaped curve: at high temperatures the pain ratings are already 10 and further increases don't result in more pain. With neuropathic or inflammatory pain, a person will often feel pain at lower temperatures. The experience of pain in response to a normally non‐painful stimulus is called: allodynia. This same person may feel more pain in response to stimuli that were previously painful, this is called hyperalgesia (see Glossary).

Figure 3.3 Stimulus response curve: normal and abnormal pain perception.

In summary, a mechanism‐based classification of pain organizes the clinical approach to the patient with pain and is effective for understanding symptoms, and ultimately planning a diagnostic work up, devising a successful treatment plan, and guiding the patient to effective self‐management.

References

1 Devor, M. (2013). Neuropathic pain: pathophysiological response of nerves to injury. Chapter 61. In: Wall and Melzack’s Textbook of Pain, 6e (eds. S.B. McMahon, M. Koltzenburg, I. Tracey and D. Turk). Philadelphia, PA: Elsevier Saunders.

2 Ringkamp, M., Raja, S., Campbell, J., and Meyer, R. (2013). Peripheral mechanisms of cutaneous nociception. In: Wall and Melzack’s Textbook of Pain, 6e (eds. M.M. SB, M. Koltzenburg, I. Tracey and D. Turk). Philadelphia, PA: Elsevier Saunders.