Nakane H, Ibayashi S, Fujii K, Sadoshima S, Irie K, Kitazono T, Fujishima M
Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
J Neurol Neurosurg Psychiatry. 1998 Sep;65(3):317-21. doi: 10.1136/jnnp.65.3.317.
Silent brain infarction (SBI) is of growing interest as a possible risk factor for symptomatic stroke. Although morphological characteristics of SBI have been well defined, their characteristic patterns of cerebral blood flow (CBF) and metabolism are in dispute. The purpose of this study was to elucidate CBF and metabolism in patients with SBI in relation to symptomatic stroke.
The patients underwent PET and were separated into three groups; control group (C group), with no lesions on CT (n=9, mean age 57), SBI group, with no neurological signs or history of stroke, but with ischaemic lesions on CT (n=9, mean age 63), and brain infarction group (BI group), with neurological deficits and compatible CT lesions in the area supplied by perforating arteries (n=19, mean age 56). Regional CBF, oxygen extraction fraction (OEF), cerebral metabolic rate for oxygen (CMRO2), and cerebral blood volume (CBV) were measured by PET.
Mean values for CBF to the cerebral cortex and deep grey matter were lower in the SBI group (31.6 (SD 5.8) and 34.3 (SD 6.9) ml/100 g/min, respectively) and in the BI group (30.8 (SD 5.2), 33.9 (SD 5.9), respectively) than in the C group (36.0 (SD 6.6) and 43.5 (SD 9.5), respectively). Although mean CMRO2 of deep grey matter (2.36 (SD 0.52) ml/100 g/min) was significantly decreased in the SBI group compared with the C group (2.76 (SD 0.480), p<0.01), CMRO2 of the cortical area was as well preserved in the SBI patients (2.36 (SD 0.39)) as in the controls (2.48 (SD 0.32)) with a compensatory increase of mean OEF (0.45 (SD 0.06) and 0.41 (SD 0.05), respectively).
Patients with SBI showed decreased CBF and CMRO2 in deep grey matter. On the other hand, decreased CBF with milder increased OEF, resulting in preserved CMRO2 in the cerebral cortex indicates the presence of occult misery perfusion, suggesting that patients with SBI have reduced cerebral perfusional reserves.
无症状脑梗死（SBI）作为有症状性卒中的一个潜在危险因素，日益受到关注。尽管SBI的形态学特征已得到明确界定，但其脑血流（CBF）和代谢的特征模式仍存在争议。本研究的目的是阐明SBI患者的CBF和代谢与有症状性卒中的关系。
患者接受了正电子发射断层扫描（PET），并被分为三组；对照组（C组），CT检查无病变（n = 9，平均年龄57岁）；SBI组，无神经体征或卒中病史，但CT检查有缺血性病变（n = 9，平均年龄63岁）；脑梗死组（BI组），有神经功能缺损，且在穿支动脉供血区域有符合CT表现的病变（n = 19，平均年龄56岁）。通过PET测量局部CBF、氧摄取分数（OEF）、脑氧代谢率（CMRO2）和脑血容量（CBV）。
SBI组（分别为31.6（标准差5.8）和34.3（标准差6.9）ml/100 g/min）和BI组（分别为30.8（标准差5.2）、33.9（标准差5.9））大脑皮质和深部灰质的CBF平均值低于C组（分别为36.0（标准差6.6）和43.5（标准差9.5））。尽管SBI组深部灰质的平均CMRO2（2.36（标准差0.52）ml/100 g/min）与C组（2.76（标准差0.480））相比显著降低（p<0.01），但SBI患者皮质区域的CMRO2（2.36（标准差0.39））与对照组（2.48（标准差0.32））一样得到良好保留，且平均OEF有代偿性增加（分别为0.45（标准差0.06）和0.41（标准差0.05））。
SBI患者深部灰质的CBF和CMRO2降低。另一方面，CBF降低，OEF轻度升高，导致大脑皮质CMRO2得以保留，这表明存在隐匿性灌注不良，提示SBI患者的脑灌注储备减少。
