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Abstract and Introduction
Abstract
Neuropathic pain (NP) develops as a consequence of a lesion or disease affecting the somatosensory pathways in the peripheral or central nervous system, and occurs in many neurological diseases (eg, peripheral neuropathy, radiculopathy, spinal cord injury, stroke and multiple sclerosis). It affects 6%–8% of the general population and its impact on quality of life, mood and sleep exceeds the burden of its causative pathology. A peculiar feature of NP is the coexistence of negative and positive symptoms and signs, reflecting loss-of-function and gain-of-function of the somatosensory system, respectively. NP has long been considered a difficult clinical issue because of the lack of a diagnostic gold standard and the unsatisfactory response to treatment. In recent years, a redefinition, diagnostic algorithm, and some guidelines on diagnosis and treatment of NP have been published. This review offers an updated overview on the definition, pathophysiology, clinical evaluation, diagnosis and treatment of NP and focuses on some of the most frequent NP conditions. We intend to help overcome uncertainties on NP and bridge the gap between evidence based medicine and the real clinical world.
Introduction
Neuropathic pain (NP) affects 6%–8% of the general population and has a great impact on the patients' quality of life and disability. While these epidemiological figures suggest that NP is endemic, with a prevalence similar to that of diabetes mellitus and asthma, NP is still considered difficult to diagnose and treat by the general practitioners and by pain and neurology specialists. The recent redefinition and diagnostic algorithm and the guidelines on diagnosis and treatment of NP may help overcome these uncertainties and bridge the gap between evidence based medicine and the real world ( Table 1 ).
The International Association for the Study of Pain (IASP) stipulated that NP is initiated or caused by a primary lesion or dysfunction in the nervous system. However, this classical definition lacked pathophysiological and anatomical specificity because it did not specify what fell under the umbrella term dysfunction, and included patients with pain secondary to motor disorders (eg, spasticity, dystonia). To overcome these limitations, the Neuropathic Pain Special Interest Group of the IASP (NeuPSIG) recently redefined NP as arising as a direct consequence of a lesion or disease affecting the somatosensory system. According to this new definition, some conditions (eg, fibromyalgia, complex regional pain syndrome type 1) which were traditionally defined as putative NP according to the classical IASP definition should not be considered as such (Table 2).
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Table 2.
NP syndromes according to the IASP classical definition and the NeuPSIG revised one
We favour the NeuPSIG redefinition because it is more specific than the IASP one and offers a diagnostic grading system (see below), which is similar to those used for other neurological diseases (eg, Alzheimer's disease, Parkinson's disease, multiple sclerosis, motor neurone disease), but there is no consensus on which NP definition is better.
NP syndromes can be divided into those that are peripheral or central, based on the anatomical location of the causative lesion or disease ( Box 1 ).
The pathophysiology of NP involves both the peripheral and the central nervous systems. The term peripheral sensitisation indicates changes in the excitability of the peripheral nerve and the dorsal root ganglion, and central sensitisation includes changes in the spinal cord neurones, the descending pain-controlling systems and abnormal brain plasticity ( Table 3 ).
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