malnutrition was described in detail in case reports from Far East prisoners of war during World War II, most likely caused by deficiency of B vitamin, and acute or subacute forms may be seen as complications to nutrient deficiencies associated with weight loss, eating disorders, and bariatric surgery. There may be multiple causes of PPN in the same patient, and in many patients, the etiology remains unknown (Lin et al., 2022). Pain may be the first symptom of neuropathy, but often the onset is insidious, starting with paresthesia and eventually dysesthesia or pain. The pain is often an ongoing squeezing, pricking, or burning pain, and evoked types of pain are less common. Depending on the affected nerves, there may be decreased reflexes, weakness, and autonomic changes. The most common form is a symmetric length-dependent polyneuropathy with symptoms in the feet, progressing proximally affecting the lower legs and hands (Qureshi et al., 2022). A specific acute form of polyneuropathy is seen after abrupt improvement in glycemic control in patients with diabetes and poor glycemic control. The pain is typically a severe burning pain accompanied by hyperalgesia, allodynia, and autonomic abnormalities. Little is known about underlying mechanisms. Another type of acute polyneuropathy is seen after treatment with the chemotherapeutic agent oxaliplatin, which causes an acute partly reversible neuropathy in almost all patients and a chronic length- dependent sensory neuropathy in only a smaller proportion. Postherpetic neuralgia Postherpetic pain (PHN) is directly related to a bout of herpes zoster onset. This pain persists for more than 3 months after herpes zoster onset. It occurs in 5–20% of patients with herpes zoster and more frequently in the elderly, and while it resolves over time in some patients, it may become chronic and persistent in a significant proportion. Both the live-attenuated and the adjuvant subunit herpes zoster vaccine reduce the 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 pain 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 ),
The underlying pathogenesis of chronic polyneuropathy has been extensively studied and can be divided into effects on the dorsal ganglion neuron, the axon, and the myelin sheath or Schwann cells. The mechanisms are diverse and include endothelial abnormalities, disrupted Schwann cell function, capillary dysfunction, breakdown of the blood-nerve barrier, apoptosis, elevated oxidative stress, direct toxic effects, mitochondrial DNA damage, loss of neurofilament polymers, impaired axonal transport, and microtubule function (Loscher et al., 2020). Less is known from clinical studies about the risk and mechanisms of pain in those with chronic polyneuropathy and why some patients remain pain-free despite a similar degree of polyneuropathy. A few possible molecular mechanisms that may underlie the neuronal hyperexcitability and ongoing activity within sensory neurons in chronic painful polyneuropathy have been proposed. These include altered expression of ion channels and receptors, increased expression of reactive metabolites such as methylglyoxal, altered neurotransmitter release, and inflammatory factors, which are further described in Section VI, and the possible role of genetic variants in genes encoding sodium channels in Section VII. Clinical studies also suggest that patients with PPN have changes in spinal and ventrolateral periaqueductal gray-mediated pain modulatory systems, altered brain connectivity, and structural brain changes (Diaz et al., 2022). 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 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). 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.
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
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