MRI DEMONSTRATION AND CT CORRELATION OF THE BRAIN IN PATIENTS WITH IDIOPATHIC INTRACEREBRAL CALCIFICATION
MRI DEMONSTRATION AND CT CORRELATION OF THE BRAIN IN PATIENTS WITH IDIOPATHIC INTRACEREBRAL CALCIFICATION
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DOI：
10.1007/bf02033355
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发表时间：
1994-05-01
影响因子：
6
通讯作者：
TADMOR, R
中科院分区：
文献类型：
--
作者：
AVRAHAMI, E;COHN, DF;TADMOR, R
22例年龄36-63岁的患者根据CT上意外的基底节广泛钙化的存在被诊断为患有法尔综合征。即使与其他脑区钙化相关，主要诊断标准仍然是基底节钙化大于800 mm 2。甲状旁腺素、血清钙、磷正常值排除高钙血症和甲状旁腺功能低下。临床上排除了线粒体CNS疾病。所有患者均行MRI、CT及神经系统检查。患者被分为两组：神经系统无症状组（第1组）和神经系统有症状组（第2组）。T2加权序列显示高信号区在所有的患者涉及的白色和灰质的大脑。第1组的高信号病变明显小于第2组。与CT显示的钙化相比，神经系统症状与T2加权MR图像上的高信号相关性更好。MRI T2加权高信号与CT显示钙化的部位不同。在15例痴呆患者中，整个半卵圆中心的白色物质呈双侧高信号。另3例轻偏瘫患者在T2加权序列上显示轻偏瘫侧对侧内囊高信号区。高信号T2可能反映了大脑中缓慢进行的代谢或炎症过程，随后钙化，可能是观察到的神经功能缺损的原因。
Twenty-two patients aged 36-63 years were diagnosed as having Fahr's syndrome on the basis of the presence on CT of unexpected extensive calcification of the basal ganglia. Even when associated with calcification of other brain areas, the main diagnostic criterion remained basal ganglia calcification larger than 800 mm2. Normal values of parathormone, serum calcium and phosphorus excluded hypercalcaemia and hypoparathyroidism. Mitochondrial CNS disease was excluded clinically. MRI and repeated CT and neurological examination were performed in all of the patients. The patients were divided into two groups: neurologically asymptomatic (group 1) and neurologically symptomatic (group 2). T2-weighted sequences demonstrated hyperintense areas in all of the patients involving the white and the grey matter of the brain. In group 1 the hyperintense lesions were significantly smaller than in group 2. The neurological symptoms correlated better with the hyperintensities on T2-weighted MR images than with the calcification demonstrated on CT. Hyperintensities in T2-weighted MRI and the areas shown by CT to have calcification had different locations. In 15 patients with dementia, the white matter of the entire centrum semiovale was bilaterally hyperintense. In another 3 patients with hemiparesis, hyperintense areas in the internal capsule, contralateral to the side of hemiparesis, were demonstrated in the T2-weighted sequence. The hyperintense T2 signals may reflect a slowly progressive, metabolic or inflammatory process in the brain which subsequently calcifies and are probably responsible for the neurological deficit observed.