TYPES AND CLASSIFICATION OF PAIN
In modern medicine, pain is essentially classified into three broad types—neuropathic, nociceptive, and inflammatory. Neuropathic pain Pain following injury to the nervous system has been known under different headings such as nerve injury pain, neuralgia, deafferentation pain, neurogenic pain, and central pain. However, in most instances and now also recognized by the International Association for the Study of Pain (IASP), the term neuropathic pain is used to avoid any postulated mechanism or a specific anatomical location of the lesion. The history of neuropathic pain reports is long with contributions from many extraordinary and exceptional scientists over the last century. Neuropathic pain is commonly described as a nerve injury or nerve impairment and is often associated with allodynia. Allodynia is a central pain sensitization that is a result of repetitive non-painful stimulation of the receptors. It triggers a pain response from a stimulus that is deemed as non-painful in normal conditions, due to the sensitization process from said repetitive stimulation. This condition can be described as “pathologic” pain because neuropathic pain serves no purpose in terms of a defense system for our body, and the pain could be in the form of continuous sensations or episodic incidents. The major causes of this type of pain could be primarily due to inflammation or metabolic diseases, such as diabetes, trauma, toxins, tumors, primary neurological diseases, and herpes zoster infection. Central sensitization plays a rather vital role in this process. Neuropathic pain can be caused by damage to the nerve, affecting the somatosensory nervous system, and may be generated by disorders of the PNS or CNS (Finnerup et al., 2021). The neurochemistry of the damaged axons can be altered due to the initiations of complex reactions upon compression, stretching, or transaction of the periphery nerves, followed by a spontaneous hyper-excitability on the site. During neuropathic pain, nociceptors demonstrate a dynamic expression of ion channels, such as Nav channels. Nav channels are the major channels in the regulation of the neuronal excitability, initiation, and propagation of the action potentials. The Na+ current in the dorsal root ganglion (DRG) can be classified into three types, namely, fast tetrodotoxin-sensitive (TTX-S), slow tetrodotoxin- resistant (TTX-R) with high-activation thresholds, and persistent TTX-R with lower activation thresholds. TTX is a potent neurotoxin and acts as a Nav channel blocker whereby it is binding with the Nav channels, inhibiting the firing of action potentials generated in the neurons. There is no gold standard or a specific set of methods or biomarkers that can document neuropathic pain. Certain neuropathic pain conditions like postherpetic neuralgia, painful diabetic neuropathy, and central poststroke pain can pose diagnostic problems, but the underlying cause is obvious. For certain mixed conditions, it may be even more
This classification is largely based on symptoms, syndromes, and mechanisms.
difficult to delineate the boundaries between neuropathic and non-neuropathic pain. Most patients with neuropathic pain complain of ongoing or intermittent spontaneous pain. Although any pain descriptor may apply, neuropathic pain is often described as burning, shooting, pricking, pins and needles, squeezing, or freezing pain (Zhang et al., 2022). The spontaneous pain is sometimes dominated by intermittent electric-shock- like pain paroxysms either alone or in addition to ongoing pain. As a consequence of the nervous system lesion, there may be nonpainful abnormal sensations. These include dysesthesia, which is unpleasant abnormal sensations, and paresthesia, which are abnormal sensations that are not considered unpleasant. Both may occur spontaneously or be evoked. Evoked types of pain may occur in addition to spontaneous pain and rarely as the only pain manifestation. Patients most often complain of touch-evoked or cold- evoked pain. On examination, allodynia (pain due to a stimulus that does not normally provoke pain) and hyperalgesia (increased pain from a stimulus that normally provokes pain) to mechanical or thermal stimuli can be found in addition to sensory loss. There may be aftersensations, which are pain continuing after stimulation has ceased; hyperpathia, an abnormal and often explosive painful reaction to a stimulus, especially a repetitive stimulus, in addition to an increased threshold; and referred sensations with the referral of pain or nonpainful sensations to denervated areas elicited by stimulation of adjacent body areas. A poor association between self-reported evoked pain and gain on quantitative sensory testing is well- known, and the discrepancy is also documented between findings on the bedside and quantitative sensory testing. The reasons for this may be that the tests are inadequate to capture allodynia and that the symptoms sometimes occur intermittently and therefore may not be present at the examination (Kumari et al., 2022). Spontaneous pain often occurs without any evoked pain, for example, in painful polyneuropathy (PPN) and complete spinal cord injury, and evoked pain may rarely occur without any spontaneous pain. This suggests that evoked and spontaneous pain are caused by different mechanisms, or by overlapping mechanisms, but preservation or loss of specific afferent fibers determines the presence or absence of evoked pain. Several studies in postsurgical pain, postherpetic neuralgia (PHN), and central neuropathic pain suggest that early evoked pain or hypersensitivity predicts the later development of neuropathic pain, suggesting that there may be shared underlying mechanisms (Bruna et al., 2020). See Figure 3.
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