Canavero S, Bonicalzi V
Department of Neurosciences, Ospedale Molinette, Turin, Italy.
Pain. 1998 Feb;74(2-3):109-14. doi: 10.1016/s0304-3959(97)00089-4.
Recent evidence suggests that central pain, i.e., pain due to central nervous system damage, may be due to a deranged neurotransmission between the sensory thalamus and sensory cortical areas. Central pain can be controlled either by opposing glutamate neurotransmission or potentiating GABAergic transmission. It is speculated that a relative hypofunction of the GABAergic inhibition both at thalamic and cortical levels leads to a sectorial excitatory hypertonus in those same areas. A blend of the two should mark each patient. A pharmacological dissection approach is provided that should optimize the treatment, up to now globally poor, of central pain.
最近有证据表明，中枢性疼痛，即由中枢神经系统损伤引起的疼痛，可能是由于感觉丘脑和感觉皮质区域之间的神经传递紊乱所致。中枢性疼痛可以通过对抗谷氨酸能神经传递或增强GABA能传递来控制。据推测，丘脑和皮质水平的GABA能抑制相对功能减退会导致这些相同区域的局部兴奋性亢进。两者的结合应是每个患者的特征。本文提供了一种药理学剖析方法，该方法应能优化目前总体效果不佳的中枢性疼痛的治疗。
