Jurna I, Zenz M
Institut für Pharmakologie und Toxikologie der Universität des Saarlandes, W-6650, Homburg/Saar, Bundesrepublik Deutschland.
Schmerz. 1992 Jun;6(2):146-9. doi: 10.1007/BF02528134.
The anticonvulsants, carbamazepine, clonazepam, phenytoin, and valproic acid are capable of depressing attacks of shooting pain in neuralgia. Shooting pain is perceived in trigeminal, intercostal, and other neuralgias, as a consequence of infectious diseases such as herpes zoster, and in the course of polyneuropathies of various causes. It is due to injury of nociceptive afferents, which generate bursts of activity in response to appropriate environmental changes. The anticonvulsant agents have no analgesic property per se, so that background pain remains unchanged. The depression of shooting pain results from the anticonvulsant action of the compounds. Both carbamazepine and phenytoin block synaptic transmission of neuronal hyperactivity by a direct depressant action that includes reduction of sodium conductance and by activation of inhibitory control. Clonazepam and valproic acid act by enhancing GABA-mediated inhibition of synaptic transmission. Carbamazepine is by far the most widely used compound; phenytoin, clonazepam, and valproic acid are not so popular because of their side effects.
抗惊厥药物卡马西平、氯硝西泮、苯妥英和丙戊酸能够抑制神经痛中的刺痛发作。刺痛见于三叉神经痛、肋间神经痛和其他神经痛,可由带状疱疹等传染病引起,也可在各种原因导致的多发性神经病过程中出现。它是由于伤害性传入神经受损,这些神经在适当的环境变化时会产生一连串的活动。抗惊厥药物本身没有镇痛特性,因此背景疼痛保持不变。刺痛的抑制是由于这些化合物的抗惊厥作用。卡马西平和苯妥英通过直接抑制作用阻断神经元过度活动的突触传递,这种直接抑制作用包括降低钠电导和激活抑制性控制。氯硝西泮和丙戊酸通过增强GABA介导的突触传递抑制作用来发挥作用。卡马西平是目前使用最广泛的化合物;苯妥英、氯硝西泮和丙戊酸由于其副作用而不太受欢迎。