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      What do general neurologists need to know about neuropathic pain? Translated title: O que os neurologistas gerais devem saber sobre dor neuropática?

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          Abstract

          Neuropathic pain (NP) is defined as pain caused by lesion or dysfunction of the somatosensory system, as a result of abnormal activation of the nociceptive pathway (small fibers and spinothalamic tracts). The most common causes of this syndrome are the following: diabetes, post-herpetic neuralgia, trigeminal neuralgia, stroke, multiple sclerosis, spinal cord injury, HIV infection, cancer. In the last few years, the NP has been receiving special attention for two main reasons: (1) therapeutical refractoriness of a variety of pain syndromes with predominant neuropathic characteristics and (2) the development of diagnostic tools for neuropathic pain complaints. The present review article provides relevant information on the understanding and recognition of NP, as well as evidence-based therapeutic approaches.

          Translated abstract

          A dor neuropática (DN) é definida como dor causada por lesão ou disfunção do sistema somatossensitivo, como resultado da ativação anormal da via nociceptiva (fibras de pequeno calibre e trato espinotalâmico). As principais causas desta síndrome são: diabetes, neuralgia pós-herpética, neuralgia trigeminal, acidente vascular encefálico, esclerose múltipla, trauma raquimedular, infecção por HIV, câncer. Nos últimos anos, a DN vem recebendo especial atenção por dois motivos principais: (1) refratariedade terapêutica de várias síndromes dolorosas com componentes neuropáticos predominantes e (2) desenvolvimento de ferramentas diagnósticas para o reconhecimento deste tipo de dor. O presente artigo de revisão fornece informações relevantes para o entendimento e reconhecimento da DN, bem como de abordagens terapêuticas baseadas em evidência.

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          Most cited references55

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          Descending control of pain.

          Upon receipt in the dorsal horn (DH) of the spinal cord, nociceptive (pain-signalling) information from the viscera, skin and other organs is subject to extensive processing by a diversity of mechanisms, certain of which enhance, and certain of which inhibit, its transfer to higher centres. In this regard, a network of descending pathways projecting from cerebral structures to the DH plays a complex and crucial role. Specific centrifugal pathways either suppress (descending inhibition) or potentiate (descending facilitation) passage of nociceptive messages to the brain. Engagement of descending inhibition by the opioid analgesic, morphine, fulfils an important role in its pain-relieving properties, while induction of analgesia by the adrenergic agonist, clonidine, reflects actions at alpha(2)-adrenoceptors (alpha(2)-ARs) in the DH normally recruited by descending pathways. However, opioids and adrenergic agents exploit but a tiny fraction of the vast panoply of mechanisms now known to be involved in the induction and/or expression of descending controls. For example, no drug interfering with descending facilitation is currently available for clinical use. The present review focuses on: (1) the organisation of descending pathways and their pathophysiological significance; (2) the role of individual transmitters and specific receptor types in the modulation and expression of mechanisms of descending inhibition and facilitation and (3) the advantages and limitations of established and innovative analgesic strategies which act by manipulation of descending controls. Knowledge of descending pathways has increased exponentially in recent years, so this is an opportune moment to survey their operation and therapeutic relevance to the improved management of pain.
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            Neuronal plasticity: increasing the gain in pain.

            We describe those sensations that are unpleasant, intense, or distressing as painful. Pain is not homogeneous, however, and comprises three categories: physiological, inflammatory, and neuropathic pain. Multiple mechanisms contribute, each of which is subject to or an expression of neural plasticity-the capacity of neurons to change their function, chemical profile, or structure. Here, we develop a conceptual framework for the contribution of plasticity in primary sensory and dorsal horn neurons to the pathogenesis of pain, identifying distinct forms of plasticity, which we term activation, modulation, and modification, that by increasing gain, elicit pain hypersensitivity.
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              Comparison of pain syndromes associated with nervous or somatic lesions and development of a new neuropathic pain diagnostic questionnaire (DN4).

              Few studies have directly compared the clinical features of neuropathic and non-neuropathic pains. For this purpose, the French Neuropathic Pain Group developed a clinician-administered questionnaire named DN4 consisting of both sensory descriptors and signs related to bedside sensory examination. This questionnaire was used in a prospective study of 160 patients presenting with pain associated with a definite neurological or somatic lesion. The most common aetiologies of nervous lesions (n=89) were traumatic nerve injury, post herpetic neuralgia and post stroke pain. Non-neurological lesions (n=71) were represented by osteoarthritis, inflammatory arthropathies and mechanical low back pain. Each patient was seen independently by two experts in order to confirm the diagnosis of neuropathic or non-neuropathic pain. The prevalence of pain descriptors and sensory dysfunctions were systematically compared in the two groups of patients. The analysis of the psychometric properties of the DN4 questionnaire included: face validity, inter-rater reliability, factor analysis and logistic regression to identify the discriminant properties of items or combinations of items for the diagnosis of neuropathic pain. We found that a relatively small number of items are sufficient to discriminate neuropathic pain. The 10-item questionnaire developed in the present study constitutes a new diagnostic instrument, which might be helpful both in clinical research and daily practice.
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                Author and article information

                Journal
                anp
                Arquivos de Neuro-Psiquiatria
                Arq. Neuro-Psiquiatr.
                Academia Brasileira de Neurologia - ABNEURO (São Paulo, SP, Brazil )
                0004-282X
                1678-4227
                September 2009
                : 67
                : 3a
                : 741-749
                Affiliations
                [01] Porto Alegre RS orgnameHospital de Clínicas de Porto Alegre orgdiv1Department of Neurology Brazil
                [02] Niterói RJ orgnameFluminense Federal University orgdiv1Department of Neurology Brazil
                Article
                S0004-282X2009000400039 S0004-282X(09)06700339
                2b5fec5d-c973-432a-b03f-8ddd89726e47

                This work is licensed under a Creative Commons Attribution 4.0 International License.

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                Figures: 0, Tables: 0, Equations: 0, References: 56, Pages: 9
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                SciELO Brazil

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                treatment,dor neuropática,dor nociceptiva,diagnóstico,tratamento,neuropathic pain,nociceptive pain,diagnosis

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