Presse Med
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Neuropathic pain, following a lesion of the peripheral or primary nervous system, is characterized by a set of pathophysiologic mechanisms and a clinical expression that distinguishes it from other chronic pain, especially inflammatory pain. These two types of pain are nonetheless frequently found in the same patient. It is important to be able to recognize neuropathic pain, either isolated or associated with other chronic pain, because it requires appropriate management.
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Neuropathic pain does not always occur in a neurological context or from evident neurological causes. The diagnosis of neuropathic pain is exclusively clinical. ⋯ Neuropathic pain can be expressed clinically with spontaneous, continuous or paroxysmal pain. Screening for neuropathic pain may be facilitated by scales such as the DN4.
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Review
[Pathophysiology of neuropathic pain: review of experimental models and proposed mechanisms].
Neuropathic pain can be conceptualized as the result of an "aberrant learning" process, associated with maladaptive plasticity of the nervous system. A number of modifications of the peripheral nervous system have been described in animal models of neuropathic pain, but their relation with different symptoms in humans is far from fully understood. We note in particular ectopic discharges in damaged myelinated fibers, abnormal activity in undamaged fibers, overexpression of calcium channels increasing the release of excitatory neurotransmitters, and sympathetic sprouting towards the spinal ganglia. ⋯ Experimental allodynia and neuropathic allodynia share the activation of the cortical pain matrix as well as the bilateralization of insular activity. However, although experimental allodynia tends to increase the activity of limbic and affective networks of the perigenual and orbitofrontal cortex, in neuropathic allodynia, analgesic procedures lead to increased activity in these structures. This suggests that their role in experimental allodynia would likely be reactive and protective, and that inability to generate their activation may contribute to the clinical expression of neuropathic pain.
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Nondrug treatments of neuropathic pain should always begin at the same time as pharmacologic treatment. There are three types of nondrug treatment for neuropathic pain: physical, surgical, and "psychocorporal" and psychotherapeutic treatment. Transcutaneous electrical nerve stimulation (TENS) is a simple physical treatment that strengthens local inhibitory controls and is indicated in focal neuropathic pain when upstream stimulation is possible for a superficial sensitive nerve trunk. ⋯ Functional surgery is implanted electric stimulation--either spinal or central (encephalic)--of structures that exert inhibitory control on the pain pathways. Spinal stimulation is performed at the level of the posterior spinal cord and is indicated essentially in segmental mononeuropathies refractory to drug treatment. Central stimulation is performed at the motor cortex and is indicated for refractory central pain. "Psychocorporal" techniques (relaxation, sophrology, hypnosis) are useful to reduce anxiety and neurovegetative hypertonicity, both factors that aggravate neuropathic pain.
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Neuropathic pain remains difficult to treat. Treatments with established efficacy in several neuropathic conditions include tricyclic antidepressants, gabapentin, pregabalin and strong opioids. Duloxetine and venlafaxine, both antidepressants, and tramadol, an opioid agonist, are also known to be effective in painful polyneuropathies, while lidocaine patches produce analgesic effects, mainly in postherpetic neuralgia. Studies show that pregabalin, gabapentin and duloxetine have positive effects that improve quality of life, and anxiety, depressive, and sleep disorders.