Guirimand F, Le Bars D
Service d'anesthésie-réanimation chirurgicale, hôpital Ambroise-Paré, Boulogne, France.
Ann Fr Anesth Reanim. 1996;15(7):1048-79. doi: 10.1016/S0750-7658(96)89477-9.
Nociception is related to the mechanisms elicited by stimuli threatening the integrity of the organism. At the peripheral level, unmyelinated C fibres (C polymodal nociceptores) or fine myelinated A delta fibres are excited by noxious stimulation, directly or indirectly by inflammatory processes. Nociceptive afferent fibres terminate in the superficial laminae of the dorsal horn of the spinal cord where informations are integrated and controlled. These first synapses are modulated by excitatory amino acids (glutamate and aspartate) and many peptides (substance P, CGRP, CCK, endogenous opiods). The majority of ascending pathways involved in nociception are located in the ventrolateral controlateral quadrant of the cord (spinorelicular and spinothalamic tracts). Many supraspinal sites are activated following nociceptive stimuli, with relays in the reticular formation of the brain stem (including the subnucleus reticularis dorsalis), the ponto-mesencephalic regions (periaqueducal gray matter and parabrachial area) and thalamic sites. Amygdala and hypothamic targets could be involved in motivational reactions and neuroendocrine adaptations to a noxious event. The cingular, insular and somatosensory cortices also receive nociceptive informations. Nociceptive signals are modulated at all levels of their transmission; the more extensively studied controls are located at the spinal level. Segmental controls are inhibitory effects produced by non-noxious mechanical stimuli. Spinal signals can also be inhibited following activation of bulbopinal descending inhibitor pathways and release of serotonin, norepinephrine and, indirectly, endogenous opiods. Inhibitory controls triggered by noxious stimuli could facilitate the extraction of the nociceptive tone of informations having priority over other stimuli.
伤害感受与威胁机体完整性的刺激所引发的机制相关。在周围水平，无髓鞘的C纤维（C多模式伤害感受器）或细的有髓鞘Aδ纤维受到伤害性刺激的直接或间接兴奋，这种间接兴奋由炎症过程引起。伤害性传入纤维终止于脊髓背角的浅层，在那里信息被整合和调控。这些最初的突触受到兴奋性氨基酸（谷氨酸和天冬氨酸）以及许多肽类（P物质、降钙素基因相关肽、胆囊收缩素、内源性阿片类物质）的调节。参与伤害感受的大多数上行通路位于脊髓的腹外侧对侧象限（脊髓网状束和脊髓丘脑束）。许多脊髓上部位在受到伤害性刺激后被激活，在脑干的网状结构（包括背侧网状核）、脑桥 - 中脑区域（导水管周围灰质和臂旁区）以及丘脑部位存在中继站。杏仁核和下丘脑靶点可能参与对伤害性事件的动机反应和神经内分泌适应。扣带回、岛叶和躯体感觉皮层也接收伤害性信息。伤害性信号在其传递的各个水平都受到调制；研究得较为广泛的调控位于脊髓水平。节段性调控是由非伤害性机械刺激产生的抑制作用。脊髓信号在延髓 - 脊髓下行抑制通路激活以及5-羟色胺、去甲肾上腺素和间接内源性阿片类物质释放后也可被抑制。由伤害性刺激触发的抑制性调控可能有助于提取优先于其他刺激的伤害性信息基调。
