proportion. Both the live-attenuated and the adjuvant subunit herpes zoster vaccine reduce the risk of herpes zoster and PHN by 50–90%. Patients with PHN have reduced unmyelinated and myelinated innervation on the affected side, and a prospective study found that initial Central neuropathic pain Central neuropathic pain is pain caused by a lesion or disease of the central somatosensory nervous system. The most common conditions are spinal cord injury in which central pain develops in ~50% of patients, stroke in which 8–10% of patients develop chronic central pain, and multiple sclerosis with a prevalence of central pain of 20%. The risk of developing central poststroke pain is highest in patients with lateral medullary and thalamic infarctions, in particular lesions involving the anterior pulvinar region of the thalamus, a major spinothalamic target. Central pain develops immediately after the insult or can have a delayed onset of up to 6–12 months but rarely longer. It may resolve in some patients during the first year, but in others could tend to become chronic and life-long, sometimes with severe psychosocial and functional consequences. Central sensitization is likely the main cause of central pain and its different characteristics, including ongoing pain, allodynia, hyperalgesia, aftersensation, and temporal summation. As discussed by Gary Bennett, spontaneous pain may not always be caused by ectopic discharges in the partially preserved or deafferented central pain pathways but could in some patients result from decreased thresholds and temporal summation of stimulus-evoked pain occurring from stimuli from daily activities, that is, breathing, touch from clothes, and ambient temperature. Relief of ongoing spontaneous pain by peripheral nerve block with lidocaine in an open-label study in patients with both spontaneous and evoked central poststroke pain supports this theory. Several studies have also found that early sensory hypersensitivity predicts the later development of central Inflammatory pain The inflammatory response presents as a series of well- orchestrated physiological processes that occur after injury or infection pathology. It is characterized by five classic symptoms: redness ( rubor ), heat ( calor ), swelling ( tumor ), pain or hypersensitivity ( dolor ), and loss of function ( function lasea ). Under normal conditions, inflammation is an important protective mechanism essential for wound healing. Inflammation is particularly insidious where the peripheral and central nervous systems are involved (‘neuroinflammation’), playing a significant role in the pathogenesis of acute and chronic pain as well as chronic neurodegenerative diseases and neuropsychiatric illness. Neutrophils are usually the first respondents of an inflammatory response and gather at the site of injury via the bloodstream, followed by the release of other chemical mediators. Inflammation may lead to three major responses: hyperalgesia, allodynia, and sympathetic maintained pain. Inflammation can also induce mast cell degranulation, which subsequently leads to the release of platelet-activating factor (PAF) and stimulates the release of 5-HT from the circulating platelet (Piancone et al., 2021). The cardinal signs of inflammation include the hot inflamed site due to an increase in blood flow toward the region, redness, and swelling due to vascular permeability pain caused by the Peripheral neuroinflammatory pain Acute peripheral inflammation occurs after injury and/or infection, and it may be associated with acute inflammatory pain. After tissue damage, local macrophages release mediators that result in the so-called inflammatory
neural injury is more severe in those who develop PHN, but that pain may recover despite the only modest recovery of sensory function and reinnervation of the skin (Gossrau et al., 2021).
pain after spinal cord injury and stroke, further supporting a link between neuronal hyperexcitability and spontaneous pain (Gylfadotirr et al., 2022). Central pain can also develop in patients with a complete transection of the spinal cord, and in these patients, the pain generator must be located at rostral deafferented sites. One possible site in both complete and incomplete spinal cord injury is the neurons in the rostral part of the spinal cord. A link between at-level sensory hypersensitivity and below- level pain, the occasional pain relief by spinal transection, and the effect of dorsal root entry zone lesions on pain and high-level spontaneous and evoked neuronal activity in the rostral spinal cord support the role of this region for central pain in a subgroup of patients with spinal cord injury and central pain. Patients with brain trauma, brain tumors, and possibly Parkinson’s disease may also experience central pain. In patients with epilepsy, a seizure can trigger the experience of pain, particularly with lesions in the operculo- insular cortex (the medial part of the parietal operculum and neighboring posterior insula), an area where electrical stimulation can also trigger pain. Plexus avulsion is an injury, typical after a motorcycle accident, where the nerve root is torn from its attachment at the spinal cord, and it affects both the peripheral and central nervous systems in the transition zone. The typical symptomatology, in this case, include complaints of severe crushing pain in the deafferented hand with additional paroxysmal pain shooting down the arm. activation and sensitization of primary afferent neurons and lasting loss of function. The localized inflammatory response then induces the release of free arachidonic acid (AA) from the phospholipids, which are converted into prostaglandins (PG) via the cyclooxygenase (COX) pathways. Pain from inflammation can be further classified into two types: chronic and acute pain. Acute inflammatory pain is normally intense and occurs for a brief period, which is initiated as a response to harmful stimuli that are normally mediated by the Aδ-fibers. Leukocytes and plasma from the bloodstream are accumulated at the site of the injury to assist in the inflammatory process. However, prolonged inflammation, better known as chronic inflammatory pain , lasts beyond the expected period of healing, which is typically mediated by C-fibers. There is a progressive shift of mononuclear cells at the site of the inflammation as well. Inflammatory pain causes the increase of afferent input into the DH of the spinal cord and leads to the development of central sensitization (Ustianowska et al., 2022). There are some mediators produced at the site of injured tissue, which include 5-HT, kinins, histamine, nerve growth factors (NGF), adenosine triphosphate (ATP), PG, glutamate, leukotrienes, nitric oxide (NO), NE, and protons.
response. Inflammatory mediators acidify the tissue, which activates nociceptive primary afferent neurons and lowers their signaling thresholds. These conditions increase the sensation of pain, both peripherally and centrally.
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