Department of Neuroscience, Mario Negri Institute for Pharmacological Research, Via G. La Masa 19, 20156 Milano, Italy .
Biomark Med. 2011 Oct;5(5):607-14. doi: 10.2217/bmm.11.61.
Experimental and clinical evidence have demonstrated the increased synthesis of specific inflammatory mediators, and the upregulation of their cognate receptors in the chronic epileptic brain, indicating that some proinflammatory pathways are activated in seizure foci. Inhibition of experimental seizures by pharmacological interference with specific proinflammatory signaling, together with evidence of changes in intrinsic susceptibility to seizures in transgenic mice with perturbed inflammatory pathways, was instrumental to establish the concept that brain inflammation has a role in the etiopathogenesis of seizures. Increasing evidence also highlights the possible involvement of inflammatory processes arising in the injured brain in the development of epilepsy (i.e., in epileptogenesis). Since brain inflammation in epilepsy is not a mere epiphenomenon of the pathology but is likely involved in the mechanisms underlying neuronal hyperexcitability, the onset of seizures and their recurrence, it might be considered as a biomarker of disease development and severity, and, as such, could be used for diagnostic, prognostic or therapeutic purposes, provided that adequate noninvasive methodologies are developed to detect and quantify brain inflammation in humans.
实验和临床证据表明，在慢性癫痫大脑中，特定炎症介质的合成增加，其相应受体的表达上调，这表明一些促炎途径在癫痫灶中被激活。通过药理学干预特定促炎信号来抑制实验性癫痫发作，以及在炎症途径失调的转基因小鼠中对癫痫易感性变化的证据，有助于确立脑炎症在癫痫发病机制中的作用的概念。越来越多的证据还强调了在受损大脑中发生的炎症过程可能在癫痫（即癫痫发生）的发展中起作用。由于癫痫中的脑炎症不是病理学的单纯表象，而是可能参与了神经元过度兴奋、癫痫发作的发生和复发的机制，因此它可以被认为是疾病发展和严重程度的生物标志物，并且可以用于诊断、预后或治疗目的，前提是开发出足够的非侵入性方法来检测和量化人类的脑炎症。
