疼痛机理与临床学习班课件.pptVIP

从临床角度透视疼痛机理;;疼痛机理离我们远吗?;;分类(原因);;;手术后慢性疼痛;病理性疼痛三大表现;;定义 ;疼痛信息传递;Transduction转导（换能transducer换能器）;Nerve growth factor↗; Transmission传递;第一痛由有髓鞘的Aδ纤维传导，而第二痛则由无髓鞘的C纤维传导。选择性阻断Aδ纤维的传导可使第一痛消失（中间），而选择性阻断C纤维的传导可使第二痛消失（底部）。 ;;;Pain input to the spinal cord: lamina I ← A-delta and C fibers lamina II ← C fibers and relay it to other laminae. lamina V (wide-dynamic range neurons) ← A-delta, C and A-beta (low threshold mechanoceptors);Glu SP;freeway;疼痛的脊髓调控;中枢下行调控;中枢下行调控;;5-HT 蓝班 ↓NE ;Inhibitory Neurotransmission 1. Inhibitory interneurons or descending projections release various NTs: GABA, NE, or endogenous opioids 2. Bind receptors on presynapse of afferent pain fiber, inhibit Ca2+ channels, leading to reduced vesicle release 3. Also bind post-synaptically: can signal via G-proteins to cause K+ efflux or Cl- influx (both are hyperpolarizing);;Glu SP;nociceptors do not adapt;传入纤维持续放电可引起投射神经元的反应发生改变;;;Mechanisms of peripheral and central sensitization in neuropathic pain.;noxiousstimulus, such as an injury or disease;外周敏化Peripheral sensitization to pain:;一炎症汤“inflammatory soup”;CGRP;;PKA phosphorylates Nav1.8/1.9; PKC phosphorylates noxious stimuli receptors (TRPV, ASIC)4. Result: increased ion influx per depolarization; lowered activation threshold;Capsaicin receptor 4.purines receptorP2X3 (a ligand-gated ion channel triggered by ATP) which is selectively expressed by small-diameter sensory neurons 5.acid-sensing ion channelis rapidly activated by conditions of acidity below pH →静态不痛的机械压力刺激:用手轻压皮肤→钝痛 ;Damaged nerves;;Central sensitization;Central sensitization (WDR);触突前治疗: 1.μ-receptor agonists Opioids 2.Calcium-channel blocker: Gabapentin加巴喷丁 3.α2-receptor agonists: Clonidine 4.NA/5-HT-reuptakeblocker: TCA:阿米替林 venlafaxine文拉发辛 5. GABABagonists Baclofen巴氯酚 ;;WDR wind-up?上发条?上扬?;glial cells (brown cell), which further enhances excitability in WDR neurons by releasing cytokines and increasing glutamate levels.;CaM