A term which covers all pathological processes that affect peripheral somatic and autonomic nerves. Many disorders affect peripheral somatic nerves and induce similar clinical features. These consist of the sensation of pins and needles (paraesthesiae), loss of sensation, and muscle weakness. Very often the most distal part of the nerve in the extremities (hands and feet) is affected first or most severely. Causes include ischaemia (eg diabetes and polyarteritis), vitamin deficiencies (B and B12), alcoholism and other poisons, inflammation of the nerves (neuritis), infections such as leprosy, and some viruses. When there is widespread involvement of many nerve fibres, the condition is known as polyneuropathy.
Types
The four major forms of nerve damage are polyneuropathy, autonomic neuropathy, mononeuropathy, and mononeuritis multiplex.
Often the form of neuropathy is further broken down as to cause (see below), or other type, such as small fiber peripheral neuropathy, which is idiopathic.
Causes
Besides diabetes, the common causes of neuropathy are herpes zoster infection, toxins, alcoholism, chronic trauma (such as repetitive motion disorders) or acute trauma (including surgery), and various neurotoxins. Neuropathic pain is common in cancer as a direct result of the cancer on peripheral nerves (e.g., compression by a tumor), as a side effect of many chemotherapy drugs, and as a result of electrical injury.
Symptoms
Neuropathy often results in numbness, abnormal sensations called dysesthesias and allodynias that occur either spontaneously or in reaction to external stimuli, and a characteristic form of pain, called neuropathic pain or neuralgia, that is qualitatively different from the ordinary nociceptive pain one might experience from stubbing a toe or hitting a finger with a hammer.
Neuropathic pain is usually perceived as a steady burning and/or "pins and needles" and/or "electric shock" sensations. The difference is due to the fact that "ordinary" pain stimulates only pain nerves, while a neuropathy often results in the firing of both pain and non-pain (touch, warm, cool) sensory nerves in the same area, producing signals that the spinal cord and brain do not normally expect to receive.
Treatment of Neuropathic Pain
Neuropathic pain can be very difficult to treat.
In animal models of neuropathic pain (Bennett & Xie, Pain 33, 87-107 (1988); Seltzer et al., Pain 43, 205-18 (1990); Chung, Pain 50, 355-63 (1992); Basbaum, Pain 76, 215-22 (1998); Woolf, Pain 87, 149-58 (2000); Vadakkan et al., J Pain 6, 747-56 (2005), compounds that only block serotonin reuptake do not improve neuropathic pain. Similarly, compounds that only block norepinephrine reuptake also do not improve neuropathic pain. Compounds such as dulexetine, venlafaxine, and milnacipran that block both serotonin reuptake and norepinephrine reuptake do improve neuropathic pain. Antidepressants usually reduce neuropathic pain more quickly and with smaller doses than they relieve depression. Antidepressants therefore seem to work differently on neuropathic pain than on depression, perhaps by activating descending norepinephrinergic and serotonergic pathways in the spinal cord that block pain signals from ascending to the brain.
In general, the antidepressants seem to be most effective on continuous burning pain, while the anticonvulsants seem to work best on sudden, lancinating, "shock-like" pains that appear to involve large numbers of peripheral nerves improperly firing together.
In some forms of neuropathy, especially post-herpes neuralgia, the topical application of local anesthetics such as lidocaine can provide relief.
In some neuropathic pain syndromes, "crosstalk" occurs between descending sympathetic nerves and ascending sensory nerves. Increases in sympathetic nervous system activity result in an increase of pain; this is known as sympathetically-mediated pain.
The NMDA receptor seems to play a major role in neuropathic pain and in the development of opioid tolerance, and many experiments in both animals and humans have established that NMDA antagonists such as ketamine and dextromethorphan can alleviate neuropathic pain and reverse opioid tolerance.
Several opioids, particularly methadone, have NMDA antagonist activity in addition to their μ-opioid agonist properties that seems to make them effective against neuropathic pain, although this is still the subject of intensive research and clinical study. While lacking double blind trials, these have shown to reduce pain and improve patient quality of life particularly for chronic neuropathic pain: Interferential Stimulation;
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