Chronic acquired hepatic failure: MR imaging of the brain at 1.5 T.
Chronic acquired hepatic failure: MR imaging of the brain at 1.5 T.
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慢性获得性肝衰竭：1.5 T 下的大脑 MR 成像。
DOI：
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发表时间：
1991
期刊：
影响因子：
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通讯作者：
D. Thiel
中科院分区：
文献类型：
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作者：
J. Brunberg;E. Kanal;W. Hirsch;D. Thiel
本文报道了42例成人非威尔逊慢性肝衰竭患者在1.5 T时的脑磁共振成像结果。t1加权图像显示30例患者苍白球信号增强，21例患者壳核信号增强，而t2加权图像显示信号强度无相应改变。两例患者的自旋密度和t2加权图像显示，苍白球中心部分对称低强度与CT扫描上的钙化区域相关。在t1加权图像上，红色核周围的中脑（17/42）和四叉肌板（4/42）也出现了强度增加。3例患者在t2加权图像上显示脑桥强度增加，与临床脑干功能障碍无关。35例患者中有28例垂体前叶t1加权图像强度增高。在大脑皮层或小脑中未发现信号强度的改变。MR结果与肝脏或甲状腺功能的实验室指标、肝脏组织学诊断或MR评估时的神经系统状态无关。基底神经节、脑垂体和中脑红核周围信号强度增高是慢性肝细胞功能障碍的特征。一种尚未确定的顺磁性物质的沉积或与星形细胞细胞器增殖相关的细胞内水松弛改变被认为是这种先前描述的慢性获得性肝衰竭的MR表现的可能机制。
The results of MR imaging of the brain at 1.5 T in 42 adults with non-Wilsonian chronic hepatic failure are reported. T1-weighted images demonstrated increased signal in the globus pallidus in 30 patients and in the putamen in 21, while T2-weighted images demonstrated no corresponding alteration in signal intensity. Symmetric low intensity in the central portion of the globus pallidus on spin-density and T2-weighted images in two patients correlated with regions of calcification on CT scans. Increased intensity on T1-weighted images also occurred in the mesencephalon surrounding the red nucleus (17/42) and in the quadrigeminal plate (4/42). Three patients demonstrated increased intensity in the pons on T2-weighted images unassociated with clinical brainstem dysfunction. Increased intensity on T1-weighted images was seen in the anterior pituitary in 28 of 35 patients. Alterations in signal intensity were not demonstrated in the cerebral cortex or cerebellum. MR findings did not correlate with laboratory indices of hepatic or thyroid function, with histologic liver diagnosis, or with neurologic status at the time of MR evaluation. Increased signal intensity in the basal ganglia, pituitary gland, and mesencephalon surrounding the red nuclei is characteristic of chronic hepatocellular dysfunction. Deposition of an as yet unidentified paramagnetic substance or altered intracellular water relaxation associated with the proliferation of astrocyte cytoplasmic organelles is postulated as the likely mechanism for this previously undescribed MR manifestation of chronic acquired hepatic failure.