Disease-based classification of neuropathic pain Different pain studies have generally classified neuropathic pain based on the related underlying disease. Regarding the newly released ICD11 classification, neuropathic pain is first organized into peripheral and central neuropathic pain based on Trigeminal neuralgia This term describes a specific type of orofacial pain affecting one or more divisions of the trigeminal nerve. The diagnosis depends on the patient’s description of characteristic electric shock-like pain attacks that are abrupt in onset and termination, last a few seconds to less than 2 minutes, and occur spontaneously or evoked by innocuous stimuli at trigger zones. The trigger zones are within cutaneous or mucous trigeminal areas, and chewing, touching, tooth brushing, or washing may provoke a paroxysm. It is debated whether the spontaneous attacks are truly spontaneous or stimulus-depended attacks triggered by subclinical stimuli. The frequency of attacks varies. There is often a remission period lasting weeks to years when patients are pain- free. Despite being classified as a peripheral neuropathic pain, the lesion is often within the root entry zone, where the myelin is primarily produced by central nervous system oligodendrocytes that extend beyond the pons and transit into myelin produced by peripheral Schwann cells, and the lesion may also be in the brain stem within the central nervous system, and trigeminal neuralgia is thus sometimes a central pain condition (Chen et al., 2022). The principal underlying cause of classical trigeminal neuralgia is considered to be a vascular compression of the trigeminal nerve root in the cisternal segment, the root entry zone, or the pontine segment resulting in morphological changes and atrophy in the nerve. There is also evidence suggesting that the effect of microsurgical decompression or radiosurgery is related to more severe compression of the nerve. Electron- microscopic and immunohistochemical examinations of nerve biopsies taken during surgery for microvascular decompression have shown demyelination and myelin abnormalities as well as axonal damage, atrophy, and sprouting. The prevailing theory is that spontaneous pain paroxysms are generated by spontaneous discharges in damaged neurons with a lowered threshold Neuropathic pain secondary to peripheral nerve injury The forms of neuropathic pain classified under this heading are a heterogeneous group of neuropathic pain conditions caused by a lesion of a peripheral nerve, for instance, during surgery or because of a trauma. There is a clear link between the risk of nerve damage, for example, during surgery, and the risk of developing chronic neuropathic pain, but there is no clear association between the severity of injury and type (transecting, stretching, crushing) of nerve damage and the development of neuropathic pain. In general, it is unclear why some patients with nerve damage develop pain while others do not. Partial axonal damage including small fiber dysfunction as opposed to demyelinating damage was a risk factor in one study with iatrogenic inferior alveolar nerve injury. High intraindividual concordance for neuropathic pain in patients with bilateral amputation or thoracotomy suggests that patient-related factors play a role, and the underlying mechanisms likely involve an interplay of peripheral and central nervous system changes, and genetic and psychological factors (Kocot-Kepska et al., 2021). The most widely accepted mechanism explaining the underlying pain in posttraumatic nerve injury, including phantom and stump pain after amputation, is the ectopic impulses generated at Painful polyneuropathy The most widely reported types of painful polyneuropathy are those due to diabetes, human immunodeficiency virus (HIV), chemotherapy, and leprosy. Fabry disease, sodium channel gene mutations, autoimmune diseases, vasculitis, chronic inflammatory
the location of the lesion or disease in the peripheral or central somatosensory nervous system. Within each of these categories, pain is classified into different neuropathic pain conditions based on the underlying disease.
for repetitive firing and cross-excitation to hyperexcitable neighboring neurons. Since there may be an immediate relief of microvascular decompression and recovery of trigeminal nerve root conduction, it is suggested that the underlying cause can be a transient conduction nerve block. Functional cross- excitation between neurons may also explain pain evoked by touching trigger zones with spike activity in large, myelinated A fibers activated by touch, causing depolarization in neighboring C-neurons. Progression to severe nerve root damage is likely to cause more prominent sensory loss and possible continuous pain because of continuous ectopic discharges. Retrograde biochemical disturbances and the immune reaction of the trigeminal ganglion and inflammation may also be involved. Neuroimaging studies have also documented subtle gray and white matter loss in brain areas involved in pain perception, but it is unclear if these changes are secondary and adaptive changes to ongoing activity from focal nerve damage or if they contribute to pain (Xia et al., 2022). The unique acute response of this neuropathic pain condition to microvascular decompression, radiofrequency ablation, and other treatments targeting the nerve directly supports that the pain generator is within the damaged section of the nerve. Secondary trigeminal neuralgia is caused by neurological diseases such as a tumor or multiple sclerosis. Multiple sclerosis is the most common cause of secondary trigeminal neuralgia, and 1–5% of patients with multiple sclerosis experience trigeminal neuralgia. Secondary trigeminal neuralgia in multiple sclerosis commences at an earlier age and is more often bilateral and is reported to be more severe and intractable than primary trigeminal neuralgia with reduced length and duration of remissions, fewer identifiable pain triggers, and more impact on quality of life. the site of nerve injury or the DRG. This is supported by the temporary effect of surgical removals of neuromas, which are neural sprouts developing at the proximal end of a transected nerve, and of peripheral nerve blocks on ongoing and evoked pain in peripheral nerve injury pain, including phantom pain. In human painful neuromas, an upregulation of activated p38 and elongation factors associated with translation (EFT1/2) mitogen- activated protein (MAP) kinases have been found. These may be molecular drivers of pain, as abnormal accumulation of such sodium channels can cause hyperexcitability and ectopic impulse generation (Lin et al., 2022). Low-grade inflammation and pro-inflammatory cytokines may be additional factors associated with pain after peripheral nerve injury as discussed further subsequently. Central sensitization involving the spinal cord and brain stem is likely to be involved, particularly in referred sensations and the spread of allodynia and hyperalgesia to neighboring dermatomes. Supraspinal neuroplastic changes and cortical reorganization are also seen after amputation, but the association between chronic pain and reorganization after amputation is uncertain.
demyelinating polyneuropathy, amyloidosis, alcohol, nonfreezing cold injury, and paraneoplastic syndrome are other reported causes of this type of neuropathic pain. Malnutrition and vitamin deficiency are other causes. PPN related to severe
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