Erkinjuntti T, Benavente O, Eliasziw M, Munoz D G, Sulkava R, Haltia M, Hachinski V
Department of Clinical Neurological Sciences, University of Western Ontario, London, Canada.
Arch Neurol. 1996 Apr;53(4):325-32. doi: 10.1001/archneur.1996.00550040053014.
To examine quantitatively white-matter changes at different sites in patients with definite vascular dementia and Alzheimer's disease.
Prospective clinical and neuropathological series.
University Hospital clinics (Helsinki, Finland and London, Ontario).
Twenty-two patients with a clinical and neuropathological diagnosis of vascular dementia and 20 patients with Alzheimer's disease.
The frequencies of focal white-matter lesions, arteriolosclerosis, and cerebral amyloid angiopathy were assessed. Validated ratings and cell counts were done in the subcortical U-fiber, centrum semiovale, and periventricular areas of the frontal white matter. Degrees of abnormality (none, mild, moderate, severe) were rated for spongiosis (vacuolization of white matter), état criblé (widening of perivascular spaces), myelin loss, oligodendrocyte density, axonal loss, and overall. Densities of oligodendrocytes and astrocytes (cells per square millimeter) were determined.
Patients with vascular dementia showed focal white-matter lesions and arteriolosclerosis more often than patients with Alzheimer's disease. The patients with vascular dementia also had significantly greater spongiosis (P<.001), état criblé (P=.004), myelin loss (P<.005) and overall white-matter abnormality (P<.001). Arteriolosclerosis was found in association with spongiosis but not with état criblé. Cerebral amyloid angiopathy did not appear to be related to any of the white-matter changes in patients with either vascular dementia or Alzheimer's disease. The U-fiber area showed fewer changes, and the periventricular area tended to be most affected.
In addition to focal infarcts, patients with vascular dementia showed widespread diffuse changes, including spongiosis and arteriolosclerosis, along with état criblé and myelin loss. White-matter changes in patients with Alzheimer's disease could not be related to infarction. Pathologic changes in small blood vessels are associated with diffuse white-matter changes and may have a distinct role in the genesis of vascular dementia.
定量研究确诊的血管性痴呆和阿尔茨海默病患者不同部位的白质变化。
前瞻性临床和神经病理学系列研究。
大学医院诊所（芬兰赫尔辛基和安大略省伦敦）。
22例经临床和神经病理学诊断为血管性痴呆的患者以及20例阿尔茨海默病患者。
评估局灶性白质病变、小动脉硬化和脑淀粉样血管病的发生率。在额叶白质的皮质下U形纤维、半卵圆中心和脑室周围区域进行经过验证的评分和细胞计数。对海绵状变性（白质空泡化）、筛状状态（血管周围间隙增宽）、髓鞘丢失、少突胶质细胞密度、轴突丢失及整体情况评定异常程度（无、轻度、中度、重度）。测定少突胶质细胞和星形胶质细胞的密度（每平方毫米细胞数）。
血管性痴呆患者比阿尔茨海默病患者更常出现局灶性白质病变和小动脉硬化。血管性痴呆患者的海绵状变性（P<0.001）、筛状状态（P=0.004）、髓鞘丢失（P<0.005）及整体白质异常（P<0.001）也明显更严重。小动脉硬化与海绵状变性有关，但与筛状状态无关。脑淀粉样血管病似乎与血管性痴呆或阿尔茨海默病患者的任何白质变化均无关。U形纤维区域变化较少，脑室周围区域往往受影响最大。
除局灶性梗死外，血管性痴呆患者还表现出广泛的弥漫性变化，包括海绵状变性和小动脉硬化，以及筛状状态和髓鞘丢失。阿尔茨海默病患者的白质变化与梗死无关。小血管的病理变化与弥漫性白质变化有关，可能在血管性痴呆的发生中起独特作用。
