Leys D, Pruvo J P, Parent M, Vermersch P, Soetaert G, Steinling M, Delacourte A, Défossez A, Rapoport A, Clarisse J
Hopital B, Lille Department of Neurology, France.
J Neurol Neurosurg Psychiatry. 1991 Jan;54(1):46-50. doi: 10.1136/jnnp.54.1.46.
To determine the possible role of Wallerian degeneration secondary to the grey matter neuronal loss in the pathogenesis of "leuko-araiosis", computerised tomography (CT) of the brain was studied in 98 normotensive and non diabetic subjects free of cardiac diseases: 32 with Alzheimer's disease, 36 with Parkinson's disease, eight with progressive supranuclear palsy, and 22 controls. In Alzheimer's disease, leuko-araiosis scores were greater than in control subjects. Leuko-araiosis was more prominent in anterior periventricular areas in Parkinson's disease and progressive supranuclear palsy, and in posterior periventricular areas in Alzheimer's disease. In two patients with Alzheimer's disease and leuko-araiosis, necropsy revealed diffuse white matter pallor, mild fibrillary astrocytosis, and in one patient limited hyaline thickening of small white matter vessels, without any infarction or hypertensive change. Changes were more severe in white matter close to cortical areas with a great density of neurofibrillary tangles. Leuko-araiosis was more severe or more widespread in Alzheimer's disease than in Parkinson's disease, progressive supranuclear palsy and normal ageing. Differences in the location of leuko-araiosis between the four groups might be due to differences in the location of the grey matter disorder and Wallerian degeneration rather than amyloid in Alzheimer's disease, Parkinson's disease, progressive supranuclear palsy and normal ageing. Wallerian degeneration might be another cause of leuko-araiosis in neuro-degenerative disorders beside previously reported extra-cerebral predisposing factors and amyloid angiopathy.
为了确定继发于灰质神经元丢失的华勒氏变性在“脑白质疏松症”发病机制中的可能作用，对98名无心脏病的血压正常且非糖尿病受试者进行了脑部计算机断层扫描（CT）研究：32例患有阿尔茨海默病，36例患有帕金森病，8例患有进行性核上性麻痹，22例为对照组。在阿尔茨海默病中，脑白质疏松症评分高于对照组。帕金森病和进行性核上性麻痹的脑室周围前部区域脑白质疏松症更明显，而阿尔茨海默病的脑室周围后部区域更明显。在两名患有阿尔茨海默病和脑白质疏松症的患者中，尸检显示弥漫性白质苍白、轻度纤维性星形胶质细胞增生，其中一名患者小的白质血管有局限性透明样增厚，无任何梗死或高血压改变。靠近神经原纤维缠结密度高的皮质区域的白质变化更严重。阿尔茨海默病中的脑白质疏松症比帕金森病、进行性核上性麻痹和正常衰老更严重或更广泛。四组之间脑白质疏松症位置的差异可能是由于灰质病变和华勒氏变性位置的差异，而非阿尔茨海默病、帕金森病、进行性核上性麻痹和正常衰老中的淀粉样蛋白。除了先前报道的脑外易感因素和淀粉样血管病外，华勒氏变性可能是神经退行性疾病中脑白质疏松症的另一个原因。
