Hertzer N R, Beven E G, Benjamin S P
Arch Surg. 1977 Nov;112(11):1394-1402. doi: 10.1001/archsurg.1977.01370110128015.
It is widely accepted that transient cerebral ischemia and permanent stroke frequently are caused by platelet and thrombotic cerebral emboli that originate from lesions at the carotid bifurcation. Microembolization from ulcerated atheroma during carotid dissection also offers a logical explanation for the incidence of intraoperative neurologic deficits during carotid endarterectomy. The risk of intraoperative embolization is obvious when ulcers are macroscopic; but focal cerebral ischemia associated with atheroma that appear smooth and nonulcerated usually has been attributed to decreased regional cerebral blood flow. Several endarterectomy specimens were submitted for scanning electron microscopic evaluation using X20 through X4,000 malignification. Results indicate that carotid atheroma may contain superficial ulcerations and thrombi that are not appreciated by direct inspection or conventional microscopic techniques. Electron microscopic ulcerations and intraluminal thrombi may be responsible for embolic transient ischemic attacks, spontaneous strokes, and intraoperative neurologic deficits in patients in whom gross ulcerations are absent.
人们普遍认为，短暂性脑缺血和永久性中风通常是由源自颈动脉分叉处病变的血小板和血栓性脑栓塞引起的。颈动脉夹层期间溃疡性动脉粥样硬化的微栓塞也为颈动脉内膜切除术中神经功能缺损的发生率提供了合理的解释。当溃疡肉眼可见时，术中栓塞的风险很明显；但与看似光滑且无溃疡的动脉粥样硬化相关的局灶性脑缺血通常归因于局部脑血流量减少。使用20倍至4000倍放大率提交了几份内膜切除术标本进行扫描电子显微镜评估。结果表明，颈动脉粥样硬化可能含有直接检查或传统显微镜技术无法察觉的浅表溃疡和血栓。电子显微镜下的溃疡和腔内血栓可能是导致无明显溃疡患者发生栓塞性短暂性脑缺血发作、自发性中风和术中神经功能缺损的原因。
