Hypoxic brain damage : MR imaging findings and its correlation with histological findings

我们研究了缺氧性脑病的序列磁共振成像表现，并将其与尸检的组织学结果相关联。我们回顾了6例缺氧性脑损伤患者的脑部序列磁共振成像研究。在重复的MR图像上评估信号强度和脑的形态特征的顺序变化。在另外两名尸检患者中，MR发现提示皮质板层坏死，MR发现与组织学结果相关联。磁共振成像使用1.5T Magnetom H15扫描仪(西门子，德国Erlangen)和磁头线圈。在轴位获得T1加权自旋回波序列图像，脉冲序列为500/15(重复时间[tr]毫秒/回波时间msec)和长tr自旋回波(2500/15，90)图像，矩阵256，层厚5-10 mm，视野20-25 cm。偶尔还能观察到额外的冠状面或矢状面图像。磁共振成像所见…的时间演变发病后1周内为急性期；11-19天为亚急性期；21-28天为亚急性期晚期；41天为慢性期。急性期出现脑水肿。增强T1加权像在亚急性期早期表现为皮质板层强化，平扫表现为亚急性期晚期特征性的板层高信号病变。这两个发现在组织学上都反映了皮质板层坏死。然而，我们不能在组织学检查中阐明是什么导致了T1加权图像上的层状高信号。慢性期可见皮质萎缩和延迟性进行性白质改变。缺氧性脑损伤的磁共振成像特征变化复杂但明显。可见皮质板层坏死和延迟性白质变性。较少

We investigated sequential MR imaging findings of hypoxic encephalopathy and correlated them with histological findings at autopsy. We retrospectively reviewed sequential MR imaging studies of the brain in 6 patients with hypoxic brain damage. Sequential changes in signal intensity and morphological features of the brain were evaluated on repeated MR images. In the other two autopsied patientnts who had MR findings suggestive of cortical laminar necrosis, MR findings were correlated with histological findings. MR imaging was performed with a 1.5-T Magnetom H15 scanner (Siemens, Erlangen, Germany) with a head coil. T1-weighted spin-echo images, with a pulse sequence of 500/15 (repetition time [TR] msec/echo time msec) and long TR spin-echo (2500/15,90) images were obtained in the axial plane, with a 256^<**>256 matrix, a 5-10-mm section thickness, and a field of view of 20-25 cm. Occasionally, additional coronal or sagittal images were obtined. Temporal evolution of MR imaging findings … More was arbitrarily divided into frou morphological stages : acute stage, within 1 week after the onset ; early subacute stage, days 11-19 ; late subacute stage, days 21-28 ; and chronic stage, days 41 onward.Involvement of the watershed zones in the parietooccipitotemporal cortex was most frequent. Cerebral edema was seen in the acute stage. Enhanced T1-weighted images showed cortical laminar enhancement in the early subacute stage ; unenhanced T1-weighted images revealed characteristic laminar hyperintense lesions in the late subacute stage. Both of these findings reflected cortical laminar necrosis at histology. However, we could not elucidate at histological examination what caused the laminar hyperintensity on T1-weighted images. In the chronic stage, cortical atrophy and delayd but progressive white matter changes were seen. Changes in MR imaging features of hypoxic brain damage are complex but distinct. Cortical laminar necrosis and delayd white matter degeneration can be delineated. Less