摘要
缺血所致神经元和其他神经细胞的死亡即缺血性脑梗死。它的发生和发展是一个动态、复杂而有序的过程。脑血流量下降达正常值的１５％～２０％以下时，神经细胞的Ｎａ~＋ ／Ｋ~＋－ＡＴＰ酶泵功能发生障碍，细胞内外离子平衡被打破，钠和水流入细胞内，导致神经元细胞毒性水肿，造成早期渗透压性细胞溶解。ＮＭＤＡ受体持续兴奋，引起大量钙内流并激活一系列酶和产生细胞毒性自由基，导致神经细胞迟发性死亡。各期脑梗死的影像学表现如下：１超急性（＜６ｈ），常规ＣＴ和ＭＲＩ常阴性，部分病例可以出现以下急性期所显示的ＣＴ和ＭＲＩ表现，唯十分轻微。ＭＲＩ弥散加权成像（ＤＷＩ）呈高信号，ＣＴ和ＭＲＩ灌注成像（ＰＷＩ）呈低灌注状态；２、急性期（６～７２ｈ）， ＣＴ可出现动脉高密度征、局部脑肿胀征和脑实质密度减低征。 ＭＲ ＴＩＷＩ呈低信号， Ｔ２ＷＩ和ＦＬＡＩＲ呈高信号；ＤＷＩ呈高信号，ＰＷＩ呈低灌注；血管内可有增强现象； ３．亚急性期（７２ｈ～１０天），常规ＣＴ和ＭＲＩ表现同急性期，此期ＤＷＩ梗死区可呈低信号，ＰＷＩ可呈低灌注；４慢性期（＞１１天），ＣＴ呈低密度；Ｔ１ＷＩ呈低信号，Ｔ２ＷＩ呈高信号，ＦＬＡＩＲ呈低信号，周边胶质增生带呈高信号，ＤＷＩ呈低信?
Cerebral infarct is defined as death of neurons and other brain cells caused by cerebral ischemia. Ischemic neuronal injury occurs through mechanisms directly related to the initial ischemic event. The cerebral ischemia can trigger a cascade of events leading to further neuronal cell death through amplification of a variety of secondary pathologic processes set in motion by ischemia. When the cerebral blood flow decreases to 15-20% of normal value, the dysfunction of Na^+ /K^+ - ATP ionic pump occurs. The failure to maintain ionic equilibrium results in a net flux of sodium and water from the extracellular space into the intracellular space, that is the so-called cytotoxic edema. The influx of sodium and water causes rapid phase of osmotic lysis or death of some neurons. When NMDA receptors are activated continueously, massive influx of calcium results in the activation of a series of related enzymes and overproduction of toxic free radicals, thus causes the delayed neuronal cells death. Imaging appearances in different stages of cerebral infarct: 1. Hyperacute infarct (<6h): Routine CT and MRI usually are negative, but sometimes may show some subtle changes which are more obvious in acute infarct. MRI DWI appears as a high signal area. CT and MRI PCI presents as a low perfusion area. 2. Acute infarct (6 - 72h): Plain CT scan can show hyperdence brain artery sign, hypodense parenchymal sign and localized brain swelling sign. MRI TIWI and T2WI (including FLAIR) appear as low signal area and high signal area separately. After injection of Gd-DTPA vascular enhancement can be seen. The appearances of MRI DWI and PCI are similar to which showed in hyperacute infarct. 3. Subacute infarct (72h-10d): The findings of routine CT and MRI and MRI PWI are same as acute infarct. MRI DWI appears as low signal area. 4. Chronic infarct (>11d): CT presents as a low density area. MRI TIWI and T2WI appear as low sighal area with a high signal rim which represents a zone of gliosis. MRI DWI shows a low signal area.
出处
《中国医学计算机成像杂志》
CSCD
2000年第1期2-36,共35页
Chinese Computed Medical Imaging
