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 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 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 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 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 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
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.
impulses generated at 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. 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. 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).
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
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