Presse Med
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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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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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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.