无认知障碍主诉的老年人的认知功能与磁共振改变及其关系研究
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摘要
研究背景
随着年龄的增长,无认知功能障碍的老年人的头颅磁共振可呈现不同程度脑萎缩、腔隙性脑梗塞和脑白质病变,目前临床医生难以解释此三种影像学改变是否影响及如何影响认知功能。近年来国内外以痴呆患者或非痴呆老人为研究对象,发现脑萎缩、腔隙性脑梗塞和脑白质病变与认知功能之间存在相关性,此外,全脑萎缩与认知损害程度相关,而局部脑萎缩可表现为特定领域的认知障碍,如海马、丘脑前核和与记忆关系密切。但也有研究显示脑局部区域的认知功能有赖于总脑容量与总体认知功能之间的关系,与局部脑萎缩无关,因此脑萎缩与认知功能之间的关系尚待进一步研究。皮质下缺血性改变所致的血管性认知功能障碍以执行功能损害突出,其他认知功能保持或缺损相对较轻。但是尚无研究很好地解释其为单一病变或混合病变所致,而且少有研究同时采用多种神经心理学测验进行综合评估,难以达到全面检查不同领域的认知损害的目的。
目的
本研究通过对无认知功能障碍主诉的老年人进行多项神经心理学测试,分析其认知功能及神经影像学特点,同时探讨不同神经影像学改变,如腔隙性脑梗塞、白质病变、脑萎缩对认知功能的影响。
方法
收集广州医学院第二附属医院神经内科住院及门诊60岁至90岁无认知功能障碍主诉的老年人57例,男23例,女24例,平均年龄73.490±7.853岁,平均受教育年限8.420±2.915年,对其进行头颅磁共振扫描、神经科体格检查,同时使用简易智能精神状态量表(Mini-Mental State Examination, MMSE)进行总体认知功能筛选。采用美国国立精神卫生研究所制定的抑郁量表(Center for Epidemiologic Studies-Depression scale,CES-D)评估患者最近一周的抑郁状态。运用蒙特利尔认知评估量表(Montreal Cognitive Assessment, MoCA),根据有无轻度认知功能障碍分为MoCA正常组及MoCA异常组。所有对象均进行多种神经心理学测验,包括Fuld物体记忆测验(Fuld Object Memory Evaluation , FOM)、词语流畅性测试(Rapid Verbal Retrieve , RVR)、积木测验(Block Design , BD)、数字广度测验(Digit Span , DS)、阿尔茨海默病评定量表-认知部分的单词回忆任务( Alzheimer’s Disease Assessment Scale-Cognitive Subscale Word Recall ,ADAS-Cog-R)及数字符号测试(Digit Symbol Test , DST)等以检测记忆、执行功能及视空间结构能力。数据结果采用SPSS16.0进行统计分析。
结果
1. 57例受试者中MoCA异常组31例,MoCA正常组26例,性别分布在两组间无统计学差异(P>0.05)。MoCA异常组平均年龄为78.06±5.946岁,MoCA正常组平均年龄为68.50±6.470岁,两组间有统计学差异(P<0.05),说明年龄与认知功能下降有关。MoCA正常组与异常组间文化程度无统计学差异(P>0.05),各组中初中及初中以上文化占主要比例。高血压、糖尿病、心脏病、高血脂所占比例在MoCA异常组均较正常组高,但是两组之间无统计学差异(P>0.05);
2. MoCA正常组与异常组之间双尾状核指数和腔隙性脑梗塞个数存在统计学差异(P<0.05),两组间脑白质病变程度无统计学差异(P>0.05),MoCA异常组脑白质病变分级的平均值为1.030;
3.在影像学改变分组中,存在一种影像学改变的受试者为20例,存在两种及两种以上影像学改变的受试者为22例;
4.与影像学正常组相比,脑萎缩组DST得分较低,并存在统计学意义(P<0.05),RVR、FOM、BD、DS、ADAS-COG得分差异无统计学意义(P>0.05);
5.与影像学正常组相比,脑萎缩、腔隙性脑梗塞、白质病变混合影像学改变组RVR、FOM得分较低,存在统计学差异(P<0.05), BD、DS、ADAS-COG、DST得分差异无统计学意义(P>0.05)。
结论
1.年龄是影响无认知功能障碍主诉的老年人认知功能减退的重要因素之一;
2.我们的研究显示在无认知功能障碍主诉的老年人中,脑萎缩、腔隙性脑梗塞、白质病变混合存在的影像学改变可能可导致认知功能下降,表现在非言语性记忆及言语流畅性方面;
3.在我们的研究中,单一的脑萎缩改变可能与信息处理速度下降相关。
Background: The brain magnetic resonance imaging of ageing people without cognitive complaints is generally characteristic of cerebral atrophy, lacunar infarction and white matter lesions in various degrees. Clinicians often struggle to explain the implications of these findings to their patients. Recent studies suggested the correlation between cognitive function and these three imaging features. The degree of cognitive impairment is correlated to whole brain atrophy, and local atrophy may show special cognitive dysfunction. But it is reported that the cognition of local brain is dependent on the association between whole brain volume and general cognitive function. Vascular cognitive impairment(VCI) derived from subcortical ischemic vascular disease(SIVD) represented impairment of executive function rather than other cognitive function. However, they didn’t elucidate their single or combined effect on cognition. Moreover, various detailed neuropsychological test are rarely applied in these studies and they can’t obtain diverse domains of cognitive function.
Objective: To investigate the neuroimaging feature in aging adults without cognitive complaints, including normal people and people with asymptomatic pathology, and explore the single and combined effects of brain atrophy, lacunar infarction and white matter lesions on cognitive function in ageing adults without cognitive complaints.
Method: In a sample of 57 people ,without cognitive complaints, aged 60-90 years of neurology apartments of the second affiliated hospital of Guangzhou Medical University, cerebral magnetic resonance imaging was performed and a detailed neuro- psychological test battery applied, such as Mini-Mental State Examination(MMSE), Montreal Cognitive Assessment(MoCA), Flud Object Memory Evaluation(FOM), Rapid Verbal Retrieve(RVR), Block Design(BD), Digit Span(DS), the Alzheimer’s Disease Assessment Scale-Cognitive Subscale Word Recall(ADAS-Cog-R), Digital Symbol Test(DST). SPSS16.0 is adopted for the statistic analysis.Group differences of imaging were tested with Student’s t-test . Analysis of covariance determined the effects of imaging features on domains of cognitive function.
Result:
1. There are 26 individuals with normal cognition and 31 individuals with cognitive impairment.The average age of the abnormal cognition group is 78.06±5.946 and those of normal cognition group is 68.50±6.470,there is statistic difference(P<0.05). Gender, education degree and vascular factors (such as hyperintension, diabetes, cadiac disease and hyperlipermia) didn’t show statistic difference between normal cognition group and abnormal cognition group(P>0.05).But higher education degree accounted for a large proportion in both groups;
2.Statistic significance in the different degree of brain atrophy and lacunar infarction between normal MoCA group and abnormal MoCA group(P<0.05); while not in the degree white matter lesion between them(P>0.05);
3.Among the neuroimaging group, there are 20 individuals with single neuroimaging feature and 22 individuals with combined neuroimaging feature;
4.There is statistic difference of the scores of DST between single brain atrophy group and normal neuroimaging group(P<0.05), but no significant difference of the scores of RVR、FOM、BD、DS、ADAS-COG between them(P>0.05);
5.Both RVR, FOM scores of combined neuroimaging group were significantly lower than that of normal imaging group(P<0.05).There is no significant difference of the scores of BD、DS、ADAS-COG、DST between them(P>0.05).
Conclusion:
1.Ageing is a factor for cognitive dysfunction in older people;
2.The combined neuroimaging of brain atrophy, lacunar infarction and white matter lesion may be prone to cognitive impairment of non-verbal memory and verbal fluency than single neuroimaging lesion in this study;
3. Single brain atrophy may make effect on processing speed of information
随着年龄的增长,无认知功能障碍的老年人的头颅磁共振可呈现不同程度脑萎缩、腔隙性脑梗塞和脑白质病变,目前临床医生难以解释此三种影像学改变是否影响及如何影响认知功能。近年来国内外以痴呆患者或非痴呆老人为研究对象,发现脑萎缩、腔隙性脑梗塞和脑白质病变与认知功能之间存在相关性,此外,全脑萎缩与认知损害程度相关,而局部脑萎缩可表现为特定领域的认知障碍,如海马、丘脑前核和与记忆关系密切。但也有研究显示脑局部区域的认知功能有赖于总脑容量与总体认知功能之间的关系,与局部脑萎缩无关,因此脑萎缩与认知功能之间的关系尚待进一步研究。皮质下缺血性改变所致的血管性认知功能障碍以执行功能损害突出,其他认知功能保持或缺损相对较轻。但是尚无研究很好地解释其为单一病变或混合病变所致,而且少有研究同时采用多种神经心理学测验进行综合评估,难以达到全面检查不同领域的认知损害的目的。
目的
本研究通过对无认知功能障碍主诉的老年人进行多项神经心理学测试,分析其认知功能及神经影像学特点,同时探讨不同神经影像学改变,如腔隙性脑梗塞、白质病变、脑萎缩对认知功能的影响。
方法
收集广州医学院第二附属医院神经内科住院及门诊60岁至90岁无认知功能障碍主诉的老年人57例,男23例,女24例,平均年龄73.490±7.853岁,平均受教育年限8.420±2.915年,对其进行头颅磁共振扫描、神经科体格检查,同时使用简易智能精神状态量表(Mini-Mental State Examination, MMSE)进行总体认知功能筛选。采用美国国立精神卫生研究所制定的抑郁量表(Center for Epidemiologic Studies-Depression scale,CES-D)评估患者最近一周的抑郁状态。运用蒙特利尔认知评估量表(Montreal Cognitive Assessment, MoCA),根据有无轻度认知功能障碍分为MoCA正常组及MoCA异常组。所有对象均进行多种神经心理学测验,包括Fuld物体记忆测验(Fuld Object Memory Evaluation , FOM)、词语流畅性测试(Rapid Verbal Retrieve , RVR)、积木测验(Block Design , BD)、数字广度测验(Digit Span , DS)、阿尔茨海默病评定量表-认知部分的单词回忆任务( Alzheimer’s Disease Assessment Scale-Cognitive Subscale Word Recall ,ADAS-Cog-R)及数字符号测试(Digit Symbol Test , DST)等以检测记忆、执行功能及视空间结构能力。数据结果采用SPSS16.0进行统计分析。
结果
1. 57例受试者中MoCA异常组31例,MoCA正常组26例,性别分布在两组间无统计学差异(P>0.05)。MoCA异常组平均年龄为78.06±5.946岁,MoCA正常组平均年龄为68.50±6.470岁,两组间有统计学差异(P<0.05),说明年龄与认知功能下降有关。MoCA正常组与异常组间文化程度无统计学差异(P>0.05),各组中初中及初中以上文化占主要比例。高血压、糖尿病、心脏病、高血脂所占比例在MoCA异常组均较正常组高,但是两组之间无统计学差异(P>0.05);
2. MoCA正常组与异常组之间双尾状核指数和腔隙性脑梗塞个数存在统计学差异(P<0.05),两组间脑白质病变程度无统计学差异(P>0.05),MoCA异常组脑白质病变分级的平均值为1.030;
3.在影像学改变分组中,存在一种影像学改变的受试者为20例,存在两种及两种以上影像学改变的受试者为22例;
4.与影像学正常组相比,脑萎缩组DST得分较低,并存在统计学意义(P<0.05),RVR、FOM、BD、DS、ADAS-COG得分差异无统计学意义(P>0.05);
5.与影像学正常组相比,脑萎缩、腔隙性脑梗塞、白质病变混合影像学改变组RVR、FOM得分较低,存在统计学差异(P<0.05), BD、DS、ADAS-COG、DST得分差异无统计学意义(P>0.05)。
结论
1.年龄是影响无认知功能障碍主诉的老年人认知功能减退的重要因素之一;
2.我们的研究显示在无认知功能障碍主诉的老年人中,脑萎缩、腔隙性脑梗塞、白质病变混合存在的影像学改变可能可导致认知功能下降,表现在非言语性记忆及言语流畅性方面;
3.在我们的研究中,单一的脑萎缩改变可能与信息处理速度下降相关。
Background: The brain magnetic resonance imaging of ageing people without cognitive complaints is generally characteristic of cerebral atrophy, lacunar infarction and white matter lesions in various degrees. Clinicians often struggle to explain the implications of these findings to their patients. Recent studies suggested the correlation between cognitive function and these three imaging features. The degree of cognitive impairment is correlated to whole brain atrophy, and local atrophy may show special cognitive dysfunction. But it is reported that the cognition of local brain is dependent on the association between whole brain volume and general cognitive function. Vascular cognitive impairment(VCI) derived from subcortical ischemic vascular disease(SIVD) represented impairment of executive function rather than other cognitive function. However, they didn’t elucidate their single or combined effect on cognition. Moreover, various detailed neuropsychological test are rarely applied in these studies and they can’t obtain diverse domains of cognitive function.
Objective: To investigate the neuroimaging feature in aging adults without cognitive complaints, including normal people and people with asymptomatic pathology, and explore the single and combined effects of brain atrophy, lacunar infarction and white matter lesions on cognitive function in ageing adults without cognitive complaints.
Method: In a sample of 57 people ,without cognitive complaints, aged 60-90 years of neurology apartments of the second affiliated hospital of Guangzhou Medical University, cerebral magnetic resonance imaging was performed and a detailed neuro- psychological test battery applied, such as Mini-Mental State Examination(MMSE), Montreal Cognitive Assessment(MoCA), Flud Object Memory Evaluation(FOM), Rapid Verbal Retrieve(RVR), Block Design(BD), Digit Span(DS), the Alzheimer’s Disease Assessment Scale-Cognitive Subscale Word Recall(ADAS-Cog-R), Digital Symbol Test(DST). SPSS16.0 is adopted for the statistic analysis.Group differences of imaging were tested with Student’s t-test . Analysis of covariance determined the effects of imaging features on domains of cognitive function.
Result:
1. There are 26 individuals with normal cognition and 31 individuals with cognitive impairment.The average age of the abnormal cognition group is 78.06±5.946 and those of normal cognition group is 68.50±6.470,there is statistic difference(P<0.05). Gender, education degree and vascular factors (such as hyperintension, diabetes, cadiac disease and hyperlipermia) didn’t show statistic difference between normal cognition group and abnormal cognition group(P>0.05).But higher education degree accounted for a large proportion in both groups;
2.Statistic significance in the different degree of brain atrophy and lacunar infarction between normal MoCA group and abnormal MoCA group(P<0.05); while not in the degree white matter lesion between them(P>0.05);
3.Among the neuroimaging group, there are 20 individuals with single neuroimaging feature and 22 individuals with combined neuroimaging feature;
4.There is statistic difference of the scores of DST between single brain atrophy group and normal neuroimaging group(P<0.05), but no significant difference of the scores of RVR、FOM、BD、DS、ADAS-COG between them(P>0.05);
5.Both RVR, FOM scores of combined neuroimaging group were significantly lower than that of normal imaging group(P<0.05).There is no significant difference of the scores of BD、DS、ADAS-COG、DST between them(P>0.05).
Conclusion:
1.Ageing is a factor for cognitive dysfunction in older people;
2.The combined neuroimaging of brain atrophy, lacunar infarction and white matter lesion may be prone to cognitive impairment of non-verbal memory and verbal fluency than single neuroimaging lesion in this study;
3. Single brain atrophy may make effect on processing speed of information
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39. Dina Zekry, Charles Duyckaerts, Joel Behnin. The vascular lesions in vascular and mixed dementia:the weight of functional neuroanatomy Neurobiology of Aging 2003,24:213-219.
40. Bowler JV, Steenhuis R, Hachinski V. Conceptual background to vascular cognitive impairment [J].Alzheimer Dis Assoc Disord,1999, 13(Suppl3):S3-S37.
41.张为,周博峰,胡才友,吕渊.老年性无症状脑梗塞认知功能障碍及其影响因素[J].慢性病学杂志,2010,12(5):388-389.
42. Boone KB , Miller BL , Lesser IM , et al . Neuropsychological correlates of white-matter lesions in healthy elderly subjects. A threshold effect .Arch Neurol . 1992,49:549–554.
1. Mann DMA: Neurobiology of Aging. In Geriatric medicine and gerontology 5th edition. Edited by: Tallis R, Fillit H, Brocklehurst JC. Edinburgh:ChurchillLivingstone; 1998, 385-422.
2. Witelson SF, Beresh H, Kigar DL: Intelligence and brain size in 100 postmortem brains: sex, lateralization and age factors.Brain 2006, 129:386-398.
3. Resnick SM, Pham DL, Kraut MA, Zonderman AB, Davatzikos C: Longitudinal magnetic resonance imaging studies of older adults: a shrinking brain. J Neurosci 2003, 23:3295-3301.
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5. Fein G, DiSclafani V, Tanabe JL, Cardenas V, Weiner MW, Jagust WJ,Reed BR, Norman D, Schuff N, Kusdra L, Greenfield T, Chui H. Hippocampal and cortical atrophy predict dementia in subcortical ischemic vascular disease. Neurology. 2000, 55:1626–1635.
6. Mungas D, Jagust WJ, Reed BR, Kramer JH, Weiner MW, Schuff N,Norman D, Mack WJ, Willis L, Chui HC. MRI predictors of cognition in subcortical ischemic vascular disease and Alzheimer’s disease. Neurology.2001, 57:2229–2235.
7. Kohler S. Quantitative characterization of verbal learning deficits in patients with Alzheimer’s disease. J Clin Exp Neuropsychol. 1994, 16:749–753.
8. Laakso MP, Soininen H, Partanen K, Helkala EL, Hartikainen P, Vainio P,Hallikainen M, Hanninen T, Riekkinen PJ, Sr. Volumes of hippocampus, amygdala and frontal lobes in the MRI- based diagnosis of early Alzheimer’s disease: correlation with memory functions. J Neural Transm Park Dis Dement Sect. 1995, 9:73– 86.
9. Stout JC, Bondi MW, Jernigan TL, Archibald SL, Delis DC, Salmon DP.Regional cerebral volume loss associated with verbal learning and memory in dementia of the Alzheimer type. Neuropsychology. 1999, 13:188–197.
10. Brunetti A, Postiglione A, Tedeschi E, Ciarmiello A, Quarantelli M,Covelli EM, Milan G, Larobina M, Soricelli A, Sodano A, Alfano B.Measurement of global brain atrophy in Alzheimer’s disease with unsupervised segmentation of spin-echo MRI studies. J Mag Res Imaging.2000, 11:260–266.
11. Richard H, Donald T,Fuqiang Gao,Sandra E. Independent cognitive effects of atrophy diffuse subcortical and thalamico-cortical cerebrovascular disease in dementia.Stoke,2008, 39:822-830.
12. O’Brien JT,Paling S,Barber R,et a1.Progressive brain atrophy on serial MRI in dementia with Lewy bodies,AD,and vascular dementia.Neurology 2001;56(10):1386-8.
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17. Bower JV. The concept of vascular cognitive impairment .J Neurol Sci 2002;203-4; 11-15.
18. Gold G,Kovari E,Horrmann FR,et a1.Cognitive consequences of thalamic,basal ganglia, and deep white matter lacunes in brain aging and dementia[J].Stroke,2005, 36: 1184. 1188.
19. Norbert Schuff,An-Tao Du,Linda L.Chao,Jollll Komak W11ite matter lesions are associated with cortical atrophy mole than entorhinal and hippocarnpal atrophy . Neurobiology of Aging 2005, 26:553-559
20. de Groot JC, de Leewu FE, Oudkerk M, et al Cerebral white matter lesions and cognitive function: the Rotterdam Scan Studyl Ann Neurol, 2000, 47: 1452-1511.
21.于波.脑梗死、白质病变与血管性认知障碍的相关研究.泰山医学院硕士学位论文.
22.Stout JC, Jernigan TL, Archibald SL, Salmon DP. Association of dementiaseverity with cortical gray matter and abnormal white matter volumes in dementia of the Alzheimer type. Arch Neurol. 1996, 53:742–749.
23. Hirono N, Kitagaki H, Kazui H, Hashimoto M, Mori E. Impact of white matter changes on clinical manifestation of Alzheimer’s disease: A quantitative study. Stroke. 2000, 31:2182–2188.
24.任艳丁,王淑荣.老年性腔隙性脑梗死血管性认知障碍与病灶部位关系[J].中国血液流变学杂志,2009,19(2):220-221.
25. American Pcychian, C Assoaxuon. Diagnostic and statistical manual of mental disorders. Fourth Edition(DSM-Ⅳ)Washington DC. American Psychiatric Association, 1991, 143-147.
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38.于波.脑梗死、白质病变与血管性认知障碍的相关研究.泰山医学院硕士学位论文.
39. Dina Zekry, Charles Duyckaerts, Joel Behnin. The vascular lesions in vascular and mixed dementia:the weight of functional neuroanatomy Neurobiology of Aging 2003,24:213-219.
40. Bowler JV, Steenhuis R, Hachinski V. Conceptual background to vascular cognitive impairment [J].Alzheimer Dis Assoc Disord,1999, 13(Suppl3):S3-S37.
41.张为,周博峰,胡才友,吕渊.老年性无症状脑梗塞认知功能障碍及其影响因素[J].慢性病学杂志,2010,12(5):388-389.
42. Boone KB , Miller BL , Lesser IM , et al . Neuropsychological correlates of white-matter lesions in healthy elderly subjects. A threshold effect .Arch Neurol . 1992,49:549–554.
1. Mann DMA: Neurobiology of Aging. In Geriatric medicine and gerontology 5th edition. Edited by: Tallis R, Fillit H, Brocklehurst JC. Edinburgh:ChurchillLivingstone; 1998, 385-422.
2. Witelson SF, Beresh H, Kigar DL: Intelligence and brain size in 100 postmortem brains: sex, lateralization and age factors.Brain 2006, 129:386-398.
3. Resnick SM, Pham DL, Kraut MA, Zonderman AB, Davatzikos C: Longitudinal magnetic resonance imaging studies of older adults: a shrinking brain. J Neurosci 2003, 23:3295-3301.
4. Adam M.,Lawrence S,et al.Measuring cerebral atrophy and white matter hyper- intensity burden to predict the rate of cognitive decline in Alzheimer disease.Arch Neurol. 2008 September, 65(9): 1202–1208.
5. Fein G, DiSclafani V, Tanabe JL, Cardenas V, Weiner MW, Jagust WJ,Reed BR, Norman D, Schuff N, Kusdra L, Greenfield T, Chui H. Hippocampal and cortical atrophy predict dementia in subcortical ischemic vascular disease. Neurology. 2000, 55:1626–1635.
6. Mungas D, Jagust WJ, Reed BR, Kramer JH, Weiner MW, Schuff N,Norman D, Mack WJ, Willis L, Chui HC. MRI predictors of cognition in subcortical ischemic vascular disease and Alzheimer’s disease. Neurology.2001, 57:2229–2235.
7. Kohler S. Quantitative characterization of verbal learning deficits in patients with Alzheimer’s disease. J Clin Exp Neuropsychol. 1994, 16:749–753.
8. Laakso MP, Soininen H, Partanen K, Helkala EL, Hartikainen P, Vainio P,Hallikainen M, Hanninen T, Riekkinen PJ, Sr. Volumes of hippocampus, amygdala and frontal lobes in the MRI- based diagnosis of early Alzheimer’s disease: correlation with memory functions. J Neural Transm Park Dis Dement Sect. 1995, 9:73– 86.
9. Stout JC, Bondi MW, Jernigan TL, Archibald SL, Delis DC, Salmon DP.Regional cerebral volume loss associated with verbal learning and memory in dementia of the Alzheimer type. Neuropsychology. 1999, 13:188–197.
10. Brunetti A, Postiglione A, Tedeschi E, Ciarmiello A, Quarantelli M,Covelli EM, Milan G, Larobina M, Soricelli A, Sodano A, Alfano B.Measurement of global brain atrophy in Alzheimer’s disease with unsupervised segmentation of spin-echo MRI studies. J Mag Res Imaging.2000, 11:260–266.
11. Richard H, Donald T,Fuqiang Gao,Sandra E. Independent cognitive effects of atrophy diffuse subcortical and thalamico-cortical cerebrovascular disease in dementia.Stoke,2008, 39:822-830.
12. O’Brien JT,Paling S,Barber R,et a1.Progressive brain atrophy on serial MRI in dementia with Lewy bodies,AD,and vascular dementia.Neurology 2001;56(10):1386-8.
13. Susan D Shenkin, Carly S Rivers,Ian J Deary,John M Starr, Joanna M Wardlaw.Maximum (prior) brain size,not atrophy,correlates with cognition in community-dwelling older people: a cross-sectional neuroimaging study. BMC Geriatrics. 2009, 9:12.
14. Christensen H, Anstey KJ, Parslow RA, Maller J, Mackinnon A, Sachdev P. The brain reserve hypothesis, brain atrophy and aging.Gerontology 2007, 53:82-95.
15. Stern Y. Cognitive reserve and Alzheimer Disease. Alzheimer Dis Assoc Disord 2006, 20(3 Suppl 2):S69-S74.
16. Stern Y, Zarahn E, Habeck C, Holtzer R, Rakitin BC, Kumar A, Flynn J, Steffener J, Brown T. A common neural network for cognitive reserve in verbal and object working memory in young but not old. Cereb Cortex 2008, 18(4):959-967.
17. Bower JV. The concept of vascular cognitive impairment .J Neurol Sci 2002;203-4; 11-15.
18. Gold G,Kovari E,Horrmann FR,et a1.Cognitive consequences of thalamic,basal ganglia, and deep white matter lacunes in brain aging and dementia[J].Stroke,2005, 36: 1184. 1188.
19. Norbert Schuff,An-Tao Du,Linda L.Chao,Jollll Komak W11ite matter lesions are associated with cortical atrophy mole than entorhinal and hippocarnpal atrophy . Neurobiology of Aging 2005, 26:553-559
20. de Groot JC, de Leewu FE, Oudkerk M, et al Cerebral white matter lesions and cognitive function: the Rotterdam Scan Studyl Ann Neurol, 2000, 47: 1452-1511.
21.于波.脑梗死、白质病变与血管性认知障碍的相关研究.泰山医学院硕士学位论文.
22.Stout JC, Jernigan TL, Archibald SL, Salmon DP. Association of dementiaseverity with cortical gray matter and abnormal white matter volumes in dementia of the Alzheimer type. Arch Neurol. 1996, 53:742–749.
23. Hirono N, Kitagaki H, Kazui H, Hashimoto M, Mori E. Impact of white matter changes on clinical manifestation of Alzheimer’s disease: A quantitative study. Stroke. 2000, 31:2182–2188.
24.任艳丁,王淑荣.老年性腔隙性脑梗死血管性认知障碍与病灶部位关系[J].中国血液流变学杂志,2009,19(2):220-221.
25. American Pcychian, C Assoaxuon. Diagnostic and statistical manual of mental disorders. Fourth Edition(DSM-Ⅳ)Washington DC. American Psychiatric Association, 1991, 143-147.
26. Amar KA. Wilcock GK. Vascular demeans. Neurology. 995, 45: 1424-1425.
27. Dina Zekry,Charles Duyckaerts,Joel Behnin,The vascular lesions in vascular and mixed dementia:the weight of functional neuroanatomy Neurobiology of Aging 2003, 24: 213-219.
28. Roman GC,The Identity of dementia and Binswanger disease.Med Hypothese,1985, 16: 389-391.
29.常杰,魏文石,李亚健.腔隙性脑梗死后血管性痴呆的进程评价[J].中国临床康复,2005, 9(28): 6-8.
30. Bowler JV, Munoz DG, Merskey H, Hachinski V.Fallacies in the pathological confirmation of the diagnosis of Alzheimer’S disease.J Neurol Neurosurg Psychiatry. 1998; 64: 18-24.
31. Bernard T, Baune , Andreas Roesler , Stefan Knecht , and Klaus Berger.Single and combined effects of cerebral white matter lesions and lacunar infarctions on cognitive function in an elderly population[J]. J Gerontol A Biol Sci Med Sci ,2009, 64(1): 118–124.