Mimenza-Alvarado A J, Muñiz-Alvarez J C, Estañol-Vidal B, Téllez-Zenteno J F, García-Ramos G
Departamento de Neurología y Psiquiatría, Instituto Nacional de Ciencias Médicas y de la Nutrición Salvador Zubirán, Mexico DF, Mexico.
Rev Neurol. 2004;39(4):364-70.
The purpose of this study is to review the different studies published in the literature concerning the different physiological mechanisms involved in the genesis of painful neuropathy, as well as the diagnostic options and the different pharmacological treatments currently available.
Distinct pathologies usually condition painful neuropathy, one of the main ones being diabetes mellitus. The triggering phenomenon is often some kind of damage to the tissues that contain nervous pain receptors, which later gives rise to a release of proinflammatory molecules, and triggers a cascade of phenomena that result in disorders in the central and peripheral nervous system (peripheral and central sensitisation). These disorders usually produce clinical manifestations, such as allodynia, paresthesias, among others, and these are sometimes the sole manifestation of painful neuropathy. Diagnosis of this syndrome is at times complicated due to the involvement of thin fibres, which cannot be identified by the conventional methods used in neurophysiological studies. There is also a broad range of pharmaceuticals used in the treatment of painful neuropathy that range from tricyclic antidepressants, non-steroidal anti-inflammatory drugs, opioid analgesics, antiarrhythmics and even agents for topical use.
Diagnosis of thin fibre neuropathy is usually performed by carrying out a Quantitative Sudomotor Axon Reflex Test, quantitative sensory tests and a skin biopsy. As regards the pharmacological treatment, the new generation of anticonvulsive drugs like gabapentin seems to have advantages over the traditional pharmaceuticals, although their widespread use is still largely restricted by their cost.
本研究旨在回顾文献中发表的有关疼痛性神经病变发生过程中涉及的不同生理机制、诊断方法以及目前可用的不同药物治疗的各类研究。
不同的病理状况通常会引发疼痛性神经病变,其中最主要的一种是糖尿病。触发现象通常是对含有神经痛觉感受器的组织造成某种损伤,随后引发促炎分子的释放,并触发一系列导致中枢和周围神经系统紊乱(外周和中枢敏化)的现象。这些紊乱通常会产生临床症状,如痛觉过敏、感觉异常等,有时这些症状是疼痛性神经病变的唯一表现。由于细纤维受累,该综合征的诊断有时会很复杂,细纤维无法通过神经生理学研究中使用的传统方法识别。治疗疼痛性神经病变还使用了广泛的药物,包括三环类抗抑郁药、非甾体抗炎药、阿片类镇痛药、抗心律失常药甚至局部用药。
细纤维神经病变的诊断通常通过进行定量汗腺轴突反射试验、定量感觉测试和皮肤活检来完成。在药物治疗方面,新一代抗惊厥药物如加巴喷丁似乎比传统药物更具优势,尽管其广泛使用仍在很大程度上受到成本的限制。