European journal of pain : EJP
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Neuropathic pain represents a series of relatively uncommon chronic pain conditions, caused by lesions or dysfunctions of peripheral or central afferent pathways in the nervous system. The symptoms and signs of neuropathic pain can all be explained by a neuronal hyperexcitability at the site of the nerve lesion, which subsequently and in a dynamic fashion recruits more central sites. The manifestations of such neuronal hyperexcitability are therefore rather similar, irrespective of the causes or sites of the lesions. ⋯ Our understanding of the mechanisms underlying neuronal hyperexcitability has increased dramatically within the last decade, and accordingly, it has been suggested that pain be classified according to a mechanism-based approach. The challenge for an improved understanding of neuropathic pain--which is the key for better treatment--lies in elucidating the relationships between symptoms, signs, aetiology, anatomical lesions, and underlying mechanisms. At present, this is not a trivial task.
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"He slept less and less; they gave him opium and began to inject morphine. But this did not relieve him. The dull pain he experienced in the half asleep condition at first only relieved him as a change, but then it became as bad, or even more agonizing, than the open pain."--Tolstoy, The Death of Ivan Ilyitch. ⋯ Those who work in chronic pain are unfortunately only too aware of the problems that such pains can cause. One of the hallmarks of neuropathic pain is poor or incomplete relief with opioids. As with so many things in medicine, there is nothing novel in this realization, as the Tolstoy quotation shows.
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While it may be convenient to categorize neuropathic pain syndromes on the basis of anatomical distribution or disease state (e.g., diabetic neuropathy, radiculopathy, postherpetic neuralgia), the treatment of neuropathic pain, alone, should also consider the signs and symptoms and the underlying putative mechanisms that may then be inferred from each individual's signs and symptoms. A diagnosis-based approach to treatment may not effectively relieve a patient's pain or improve his or her quality of life, the ultimate goal of treatment. Although research that supports a symptom- and mechanism-based approach to treating neuropathic pain is ongoing and dynamic, the preclinical and clinical data available thus far form an initial rational framework within which we may attempt to target putative pain mechanisms.
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Review Meta Analysis
Anticonvulsants in neuropathic pain: rationale and clinical evidence.
Neuropathic pain, whether of peripheral or central origin, is characterized by a neuronal hyperexcitability in damaged areas of the nervous system. In peripheral neuropathic pain, damaged nerve endings exhibit abnormal spontaneous and increased evoked activity, partly due to an increased and novel expression of sodium channels. In central pain, although not explored in detail, the spontaneous pain and evoked allodynia are also best explained by a neuronal hyperexcitability. ⋯ The most common adverse effects of anticonvulsants are sedation and cerebellar symptoms (nystagmus, tremor and incoordination). Less common side-effects include haematological changes and cardiac arrhythmia with phenytoin and carbamazepine. The introduction of a mechanism-based classification of neuropathic pain, together with new anticonvulsants with a more specific pharmacological action, may lead to more rational treatment for the individual patient with neuropathic pain.