神经病学（人卫九版）9-缺血性脑血管病.ppt

* * * * * * * * * * * * * * * * 11.3 Headache attributed to disorder of eyes 11.3.1 Headache attributed to acute glaucoma 11.5 Headache attributed to rhinosinusitis 11.5 Headache attributed to rhinosinusitisNotes 11.7 Headache or facial pain attributed to temporomandibular joint disorder 12. Headache attributed to psychiatric disorderNew section in classification 12. Headache attributed to psychiatric disorderNotes 12.1 Headache attributed to somatisation disorder 12.2 Headache attributed to psychotic disorder Part 3:Cranial neuralgias, central and primary facial pain and other headaches 3. Cranial neuralgias and central causes of facial pain 13.1 Trigeminal neuralgia 13.1.1 Classical trigeminal neuralgia 13.1.2 Symptomatic trigeminal neuralgia 13.18.4 Persistent idiopathicfacial pain Previously used term: Atypical facial pain ACUTE HEADACHE IN THEEMERGENCY DEPARTMENT * 前面的专家已经讲到了，AS的发病机制，目前得到公认的有脂质浸润学说、炎症学说和脂质氧化学，这个是动脉粥样硬化形成机制的示意图，在座的各位专家已经非常熟悉这张图了 可以很清楚地看到： 首先他汀类调脂药物可以降低血液中的LDL-C水平； 同时，普罗布考抑制渗入至内膜下的LDL氧化，从源头上阻断了动脉粥样硬化的形成； 其次普罗布考抑制了动脉粥样硬化中单核-巨噬细胞粘附-穿越-增殖-退化过程的关键细胞因子，如VCAM-1， MCP-1， M-CSF等，从而抑制了泡沫细胞的形成 可以看出，抗氧化应激治疗是抗动脉粥样硬化的重要组成部分 There are a number of pathways that result in lesions causing acute myocardial infarction (AMI). On the basis of current clinical evidence, we proposethat lesions with the greatest propensity for causing myocardial infarction are those that are at least 50% stenotic on a coronary angiogram, that undergo rapid lesion pro gression, and/or that are ischemic. FFR ? fractional flow reserve; WSS ? wall shear stress Fig. 2 Top left panel illustrates a rupture-prone plaque. The lipid-rich core occupies approximately 40% of the plaque area and contains multiple cholesterol crystals. The ?brous cap is thin and in?amed with few smooth muscle cells. Plaque microvessels originating from the adventitia extend through the media into the base of the plaque, and the plaque tends to grow out-wards (expansive remodelling). Top right panel illustrates