Which vascular lesions are of importance in vascular dementia?

被引:52
作者
Esiri, MM
机构
[1] Univ Oxford, Dept Clin Neurol, Oxford, England
[2] Radcliffe Infirm NHS Trust, Dept Neuropathol, Oxford, England
来源
VASCULAR FACTORS IN ALZHEIMER'S DISEASE | 2000年 / 903卷
关键词
D O I
10.1111/j.1749-6632.2000.tb06373.x
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 [理学]; 0710 [生物学]; 09 [农学];
摘要
Most necropsy surveys of dementia have found that vascular disease is second only to Alzheimer's disease as a cause of dementia, Alzheimer's disease and cerebrovascular disease also often coexist, The purpose of the present study was to determine the nature of the cerebrovascular lesions that are most significant in producing dementia, These were analyzed in a group of cases of dementia in which only vascular pathology was present and, in particular, no more than trivial amounts of Alzheimer-type pathology were present. The cerebrovascular lesions in this group of cases were compared with those in a group of stroke cases who were nondemented and a group of elderly cases without stroke or dementia, Severe cribriform change and deep white/grey matter microinfarcts were significantly more common in the test group than in either of the control groups, whereas single macroscopic infarcts were more common in the stroke control group than either of the other two groups. Thus, microvascular deep white and grey matter lesions, but not macroscopic infarction, were significant in vascular dementia, The results of this study will be discussed in relation to the view that microvascular lesions may also contribute to dementia in subjects with more extensive Alzheimer-type pathology and thus lower the threshold at which Alzheimer-type pathology becomes clinically manifest.
引用
收藏
页码:239 / 243
页数:5
相关论文
共 20 条
[1]
NEUROPATHOLOGICAL STAGING OF ALZHEIMER-RELATED CHANGES [J].
BRAAK, H ;
BRAAK, E .
ACTA NEUROPATHOLOGICA, 1991, 82 (04) :239-259
[2]
ACE, MTHFR, factor V Leiden, and APOE polymorphisms in patients with vascular and Alzheimer's dementia [J].
Chapman, J ;
Wang, NS ;
Treves, TA ;
Korczyn, AD ;
Bornstein, NM .
STROKE, 1998, 29 (07) :1401-1404
[3]
Persistent functional deficit in multiple sclerosis and autosomal dominant cerebellar ataxia is associated with axon loss [J].
Davie, CA ;
Barker, GJ ;
Webb, S ;
Tofts, PS ;
Thompson, AJ ;
Harding, AE ;
McDonald, WI ;
Miller, DH .
BRAIN, 1995, 118 :1583-1592
[4]
Neuropathological assessment of the lesions of significance in vascular dementia [J].
Esiri, MM ;
Wilcock, GK ;
Morris, JH .
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 1997, 63 (06) :749-753
[5]
FISHER CM, 1989, J NEUROL, V236, P65
[6]
Atherosclerosis, apolipoprotein E, and prevalence of dementia and Alzheimer's disease in the Rotterdam Study [J].
Hofman, A ;
Ott, A ;
Breteler, MMB ;
Bots, ML ;
Slooter, AJC ;
vanHarskamp, F ;
vanDuijn, CN ;
Van Broeckhoven, C ;
Grobbee, DE .
LANCET, 1997, 349 (9046) :151-154
[7]
Apolipoprotein E polymorphism in patients with Alzheimer's disease, vascular dementia and ischemic cerebrovascular disease [J].
Ji, Y ;
Urakami, K ;
Adachi, Y ;
Maeda, M ;
Isoe, K ;
Nakashima, K .
DEMENTIA AND GERIATRIC COGNITIVE DISORDERS, 1998, 9 (05) :243-245
[8]
The incidence of dementia - A meta-analysis [J].
Jorm, AF ;
Jolley, D .
NEUROLOGY, 1998, 51 (03) :728-733
[9]
Declarative and procedural learning, quantitative measures of the hippocampus, and subcortical white alterations in Alzheimer's disease and ischaemic vascular dementia [J].
Libon, DJ ;
Bogdanoff, B ;
Cloud, BS ;
Skalina, S ;
Giovannetti, T ;
Gitlin, HL ;
Bonavita, J .
JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY, 1998, 20 (01) :30-41
[10]
The relationship between apolipoprotein E, dementia, and vascular illness [J].
Marin, DB ;
Breuer, B ;
Marin, ML ;
Silverman, J ;
Schmeidler, J ;
Greenberg, D ;
Flynn, S ;
Mare, M ;
Lantz, M ;
Libow, L ;
Neufeld, R ;
Altstiel, L ;
Davis, KL ;
Mohs, RC .
ATHEROSCLEROSIS, 1998, 140 (01) :173-180