CSF spaces in idiopathic normal pressure hydrocephalus: morphology and volumetry.
CSF spaces in idiopathic normal pressure hydrocephalus: morphology and volumetry.
复制标题
特发性正常压力脑积水的脑脊液空间：形态和体积。
DOI：
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发表时间：
1998
期刊：
影响因子：
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通讯作者：
T. Imamura
中科院分区：
文献类型：
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作者：
H. Kitagaki;E. Mori;Kazunari Ishii;S. Yamaji;N. Hirono;T. Imamura
目的
特发性正常压力脑积水（NPH）是导致老年人痴呆的重要原因；然而，特发性 NPH 通常很难与正常衰老和血管性痴呆区分开来，后者存在脑萎缩伴脑室扩张（空泡性脑积水或中枢性萎缩）。为了阐明特发性 NPH 中脑脊液分布的独特特征，我们使用 MR 成像来研究特发性 NPH 患者与其他痴呆患者相比的脑脊液间隙的形态特征和体积。
方法
我们通过冠状 T1 加权 MR 图像的半定量和体积分析，评估了 11 名分流反应性特发性 NPH 患者的四个脑脊液室（脑室、基底池、侧裂间隙和侧裂蛛网膜下腔）的大小。研究结果与 11 名年龄和性别匹配的阿尔茨海默病患者和 11 名血管性痴呆患者的结果进行了比较。
结果
与其他痴呆患者相比，特发性 NPH 患者的脑脊液体积显着增加，而上凸面和内侧蛛网膜下腔的脑脊液体积显着减少。特发性 NPH 患者的侧裂脑脊液体积显着大于阿尔茨海默病患者。三组的基底池容积相当。在几名特发性 NPH 患者中，在半球的凸面或内侧表面观察到局灶性扩张的脑沟。
结论
我们的结果表明，扩大的基底池和外侧裂以及局灶性脑沟扩张的结果支持而不是排除分流反应性特发性 NPH 的诊断，并表明这种情况是由外侧裂上蛛网膜下腔阻滞引起的。
PURPOSE
Idiopathic normal pressure hydrocephalus (NPH) is an important cause of dementia in the elderly; however, idiopathic NPH is often difficult to differentiate from normal aging and vascular dementias in which brain atrophy with ventricular dilatation (hydrocephalus ex vacuo or central atrophy) is present. To elucidate the distinctive features of the distribution of CSF in idiopathic NPH, we used MR imaging to investigate the morphologic features and volume of the CSF space in patients with idiopathic NPH compared with those with other dementias.
METHODS
We assessed the size of four CSF compartments (the ventricle, basal cistern, sylvian space, and suprasylvian subarachnoid space) in 11 shunt-responsive patients with idiopathic NPH by semiquantitative and volumetric analyses of coronal T1-weighted MR images. The results were compared with those in 11 age- and sex-matched patients with Alzheimer disease and in 11 patients with vascular dementia.
RESULTS
In patients with idiopathic NPH, the CSF volume was significantly increased in the ventricles and decreased in the superior convexity and medial subarachnoid spaces as compared with patients with other dementias. The sylvian CSF volume in patients with idiopathic NPH was significantly greater than in patients with Alzheimer disease. The volume of the basal cistern was comparable among the three groups. In several patients with idiopathic NPH, focally dilated sulci were observed over the convexity or medial surface of the hemisphere.
CONCLUSION
Our results indicate that findings of enlarged basal cisterns and sylvian fissures and of focally dilated sulci support, rather than exclude, the diagnosis of shunt-responsive idiopathic NPH and suggest that this condition is caused by a suprasylvian subarachnoid block.