2008Vascular dementia

Vascular Dementia

Michael J. Schneck

Top Stroke Rehabil 2008;15(1):22–26? 2008 Thomas Land Publishers, https://www.sodocs.net/doc/c610463003.html, doi: 10.1310/tsr1501-22

22

Michael J. Schneck, MD, is Associate Professor of Neurology and Neurosurgery, Loyola University Chicago, Stritch School of Medicine, Maywood, Illinois.

Vascular dementia (VaD) is the second most common form of dementia after Alzheimer’s dementia (AD). It is characterized by loss of executive function with milder memory loss as compared with AD and is associated with cerebral brain infarction or hemorrhage. Treatment is predominantly focused on cardiovascular risk factor reduction, but anticholinesterase inhibitors and memantine may play a role. The data is most robust for donepezil. Key words: anticholinesterase inhibitors,memantine, vascular dementia

C

riteria for the diagnosis of vascular dementia (VaD) were first elucidated by Roth and modified by Mayer-Gross and

colleagues in the 1950s and 1960s.1 VaD was described as a dementia with focal signs and symptoms consistent with stroke and included a waxing and waning course, emotional lability,preservation of insight, and possibly accompanying seizures. Modification of the definition included age of onset at 60–70 years;vascular risk factures including hypertension,somatic complaints, apathetic mood, irritability and restlessness; and memory decline but with preservation of intellectual powers and personality until late in the disease.1,2 Subsequently, specific criteria for VaD were defined by Hachinski et al.;they developed a semi-quantitative scale to distinguish between VaD and Alzheimer’s disease (AD).3 Gorelick et al. noted that the Hachinski score is heavily weighted toward stroke, with low scores tending to exclude VaD but high scores not ruling out a mixed VaD/AD picture.1 O’Neill also demonstrated that there is much variability in the interpretation of the individual items in the score.4Nevertheless, the tool has some utility, and a low Hachinski score is less likely to be associated with a diagnosis of VaD 4–7 (see Table 1).

Other VaD diagnostic guidelines in the Ameri-can Academy of Neurology practice parameter on dementia are the National Institute of Neurological Disorders and Stroke—Association Internationale pour la Recherche et l’Enseignement en Neuro-sciences (NINDS-AIREN) criteria, the State of Cali-fornia Alzheimer’s Disease Diagnostic and Treat-ment Centers (ADDTC) criteria, the modified

Hachinski Ischemic Score (MHIS), and the Diag-nostic and Statistical Manual of Mental Disorders, text revision (DSM-IV-TR ) criteria.6,7 The NINDS-AIREN criteria are the most specific of the criteria and are used most commonly in studies investigat-ing potential new therapies for vascular demen-tia.5,8 The criteria for VaD in all of the diagnostic guidelines is essentially mechanistic based on clinical patterns and concomitant evidence by

Table 1.Hachinski score 3

Criterion

Scale points

Abrupt onset

2Stepwise deterioration 1Fluctuating course 2Nocturnal confusion

1Relative preservation of personality 1Depression

1Somatic complaints 1Emotional incontinence 1History of hypertension 1History of strokes

2Evidence of associated atherosclerosis 1Focal neurological symptoms 2Focal neurological signs

2

Note: A total score of 0–4 is suggestive of Alzheimer’s disease,whereas a score equal to or greater than 7 suggests vascular dementia.

Vascular Dementia23

neuroimaging of lesions that suggest vascular dis-ease; whereas CT scans may be sufficient, MR imaging is preferable for elucidation of vascular pathology. The Rotterdam dementia study showed convincingly that patients with silent brain infarcts on MRI had a significantly increased risk of de-mentia; the hazard ratio for developing dementia was 2.26 (95% confidence interval [CI] 1.09–4.70).9 Additionally, Black notes that “the criteria for probable vascular dementia also require a tem-poral relationship between onset of dementia and occurrence of a stroke (arbitrarily set at 3 months), a stepwise decline in cognitive function, or a sud-den onset of dementia.”6(p21)

Just as there are different stroke subtypes mecha-nistically, there are different forms of vascular de-mentia. These include dementia due to multiple infarcts, posthemorrhagic dementia, dementia due to focal infarcts such as an infarction of the frontal lobe, subcortical dementias due to white matter disease or to subcortical hemispheric ischemia, and dementia in the context of hemorrhagic stroke.1,2,6,10 The cognitive impairment occurring as a result of global-hypoxic injury, that is, from cardiac arrest, may also be considered a form of vascular dementia. Subcortical dementias may occur as a result of is-chemia to the subcortical gray matter, and focal lesions in areas such as the anteromedial thalamus may result in marked impairment of cognition with-out focal motor or sensory deficits.6

The most common form of VaD is multi-infarct dementia; Vladimir Hachinski first described the term multi-infarct dementia.1,2 Multi-infarct demen-tia patients experience a number of small ischemic strokes that may not result in focal neurologic defi-cits. Over time, however, the cumulative damage results in cognitive decline with impairment in ac-tivities of daily living. Thus, the effects of the small strokes are not additive but rather cumulative; one small stroke plus one small stroke does not simply equal two small strokes. Sometimes patients with multi-infarct dementia may have components of AD, leading to the term mixed dementia. It can be difficult, however, to distinguish between AD and VaD. Typically, VaD has less memory impairment as compared to AD.1,2,6 VaD may progress in an apparent stepwise fashion as additional infarctions accumulate as opposed to a more gradual cognitive decline described with AD. Additionally, focal symptoms and behavioral abnormalities such as mood disorders and inappropriate laughing/crying may manifest earlier in VaD as opposed to AD. Formal neurocognitive testing may help in differen-tiating VaD and AD. VaD patients have milder im-pairment of memory with impairments in executive function such as judgment, whereas AD is associ-ated with more global memory impairments. Addi-tionally, formal neurocognitive testing may be im-portant in distinguishing the pseudo-dementia of depression in stroke patients as depression is rela-tively common post stroke (see the article by Dafer et al. in this issue for further discussion of poststroke depression).

A specific form of vascular dementia, subcortical vascular dementia, is referred to as Binswanger’s disease; it is a result of diffuse ischemic injury to the deep hemispheric white matter. This injury is presumed to result from thickening and narrowing described as lipohyalanosis in the context of ath-erosclerotic vascular injury. Binswanger’s disease patients have psychomotor retardation, memory deficits that are not as severe as AD, changes in speech, personality changes, urinary dysfunction, and gait unsteadiness. A critical distinction be-tween Binswanger’s disease and normal pressure hydrocephalus is that in Binswanger’s disease there may enlargement of the ventricles but this hydrocephalus is ex vacuo (due to loss of brain tissue) with diffuse cortical atrophy and substan-tial diffuse white matter changes on neuroimaging. Data suggest that the annual incidence of VaD may range from 20–40 per 100,000 between per-sons 60 and 69 years old to 200–700 per 100,000 in persons over age 80, with prevalence rates dou-bling every 5 years.1,2,6,10,11 As with cerebral is-chemic disease, the risk of VaD is somewhat higher for men as compared with women. After AD, VaD is the second most common form of dementia, comprising 10%–20% of all dementias. A number of series suggest that the incidence of VaD may be higher in Asian countries and Eastern European countries, possibly related to a higher incidence of stroke risk factors.1,6 Roman has suggested that VaD may be the most underdiagnosed form of dementia in the elderly and estimates a VaD preva-lence of one million persons in the United States.12

24T OPICS IN S TROKE R EHABILITATION/J AN-F EB 2008

Additionally, there is a decreased survival for VaD patients as compared to patients with AD, presum-ably related to underlying cardiovascular disease risk factors.11,13

Risk factors for VaD reflect the general risk fac-tors associated with cerebral ischemia: age, hyper-tension, diabetes, obesity, cigarette smoking, hy-perlipidemia, and cardiac disease (including coronary artery disease and cardiac arrhythmias). Persons with autoimmune disorders such as lupus or cerebral arteritis may have cognitive decline suggestive of VaD. In these patients, the progres-sion of dementia may be stabilized or even re-versed with treatment of the underlying autoim-mune disorder.5 Persons with genetic cerebrovascular disorders may also develop a VaD-like dementia. The most common form of heredi-tary stroke disorder is CADASIL (cerebral autoso-mal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) that occurs as a result of mutations of the Notch 3 gene on chro-mosome 19.14 As the disease progresses, CADASIL patients frequently develop a subcortical demen-tia. As such, dementia with white matter changes in middle-aged persons should prompt a search for the CADASIL gene in these patients and their family members.

Treatment of cardiovascular risk factors is likely to decrease the risk of VaD. In the Rotterdam Study, subjects taking antihypertensive medica-tion at baseline (n = 2,015) who were then fol-lowed for a mean of 2.2 years had a reduced incidence of dementia (adjusted relative risk, 0.76; 95% CI 0.52–1.12). The risk reduction was most pronounced for VaD with an adjusted relative risk of 0.30 (95% CI 0.11–0.99).15 Aspirin has been associated with decreased mortality in patients with dementia but neither aspirin nor any other antiplatelet agent has been shown to ameliorate cognitive decline in patients with VaD.16–18 Still, as antiplatelet agents have been shown to have ben-efit in reducing recurrent stroke; at least the use of aspirin seems appropriate in patients with silent cerebral ischemia at risk for cognitive decline.17 Even though statins have been shown to prevent both incident and recurrent cerebral ischemic stroke, the benefit of statin therapy in AD and/or VaD is as yet undefined. Because of the benefit in preventing recurrent stroke, it seems reasonable that patients with VaD be treated with statin therapy to prevent stroke or myocardial infarc-tion.19 To date, however, there is no evidence that statin therapy reduces the incident risk of demen-tia. There was a slight trend in a post hoc analysis of the Cardiovascular Health Study toward less cognitive decline in patients treated with statins, but there was no change in the risk of incident dementia in this cohort.20,21 Similarly, two other prospective cohort studies also failed to show a reduction in dementia associated with statin use.22,23 As for other agents for prevention or treat-ment of vascular dementia, Gingko biloba extract, one of the most touted herbal remedies for VaD, was subjected to a randomized trial in Maastricht, Netherlands, and failed to show any benefit in patients with VaD or AD.24

Several of the anticholinesterase inhibitors (aCHI) have been tried in VaD patients with the rationale that the aCHI drug class was previously shown to have particular benefit in executive func-tion and cognition and this is particularly impaired in VaD.6,10 To date, however, only donepezil has shown to have efficacy. In two separate random-ized trials, this agent showed improvement as compared with placebo in the Alzheimer’s Disease Assessment Scale–cognitive subscale (ADAS-cog), and there was also benefit in maintaining indepen-dent activities of daily living (ADLs).10,25,26 Rivastigmine and galantamine, however, have not demonstrated similar convincing improvements in VaD patient cognitive function.10 Whether the lack of efficacy of rivastagmine and galantamine reflects variables related to study design as opposed to the presence of a true therapeutic difference between these two agents and donepezil is unknown. Most recently, though, a 26-week randomized study of 788 VaD patients (half of whom were assigned to either galantamine or placebo) showed only a mar-ginal improvement in cognition without benefit in overall ADLs for patients in the galantamine arm.27 In regard to memantine, an N-methyl-D-aspartate antagonist that purportedly slows clinical decline in moderate to severe AD, two randomized studies showed some benefit in ADAS-cog scores for VaD patients given memantine but there was no benefit for any other of the measured cognitive, clinical, or

Vascular Dementia25

ADL parameters. 10 Cochrane reviews supported the use of donepezil for VaD and suggested that there might be some benefit for vascular cognitive impairment with rivastigmine but that larger well-designed randomized studies were necessary.28,29 Two Cochrane reviews concluded that there was insufficient evidence to support the use of galantamine and memantine, respectively, in pa-tients with VaD.30,31

In conclusion, the evidence suggests that ag-gressive cardiovascular risk factor modification should be the therapeutic mainstay for patients with vascular dementia in order to prevent recur-rent cerebrovascular events. Whether risk factor modification with antithrombotic agents or statin therapy will prevent the cognitive decline associ-ated with cerebrovascular disease remains to be determined.

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老年痴呆临床诊断与治疗试题答案

老年期痴呆的临床诊断答案 1、帕金森（叠加）综合征通常以（A）为首发症状 A、运动症状 B、幻觉或错觉 C、肢体动作不协调 D、以上都是 2、关于进行性非流利性失语语言障碍的叙述错误的是（B） A、流畅性差 B、节律正常 C、拼音异常 D、忧郁多见 3、老年变性病所致痴呆的第二常见病因（D） A、CADASIL B、额颞叶痴呆 C、SD D、路易体痴呆 4、痴呆的病因包括（D） A、变性病、血管病、感染 B、肿瘤及副肿瘤性 C、外伤、中毒 D、以上都是 5、关于进行性核上性麻痹的叙述错误的是（B） A、缓慢起病，进行性加重 B、无帕金森样表现 C、眼球运动障碍 D、中轴性肌张力障碍 6、进行性非流利性失语占FTLD的（A）% A、20 B、30 C、40 D、50 7、路易体痴呆临床特点不包括（D） A、反复出现的视幻觉 B、自发性锥体外系损害 C、病程进行性加重 D、早期记忆障碍明显 8、下列（D）以眼球活动障碍为首发症状A、阿尔茨海默病B、血管性痴呆C、额颞叶变性D、进行性核上性麻痹 9、关于语义性痴呆叙述错误的是（C）A、进行性命名不能B、词语理解受损C、影像学额叶前部萎缩D、易误诊为AD

10、痴呆的诊断方法包括（D）A、病史、躯体及神经精神检查B、神经心理学检查C、实验室及影像学检查D、以上都是老年期痴呆的鉴别诊断及病例分析答案 1、克雅氏病分（C）型A、2B、3C、4D、5 2、正压性脑积水（NPH）临床特点不包括（D）A、步态异常 B、痴呆 C、小便失禁 D、脑脊液压力异常 3、关于散发型CJD叙述错误的是（C）A、中年后发病B、进行性加重的痴呆、锥体外系损害、肌阵挛C、MRI：底节及皮层信号正常D、周期性尖慢复合波 4、关于亨廷顿舞蹈病叙述错误的是（C）A、常染色体显性遗传B、大脑皮质及新纹状体病变C、第6号染色体异常D、治疗选用丁苯那嗪 5、亨廷顿舞蹈病临床特征包括（D）A、舞蹈样不自主运动B、进行性痴呆C、多在中年起病D、以上都是 6、家族性克雅氏病占（C）% A、80－90 B、20－30 C、10 D、5 7、关于副肿瘤性边缘性脑炎叙述错误的是（B）A、机体对肿瘤抗原的自身免疫反应B、于癌症诊断之后出现C、症状可以在数周或数月内进行性加重D、颞叶内侧及相关边缘结构T2高信号 8、散发型CJD血清S100蛋白浓度（A）A、升高B、降低C、不变D、以上均可

2015.6.2 痴呆病例分析

血管性痴呆 一、病史资料 1、现病史 患者，男性，78岁，因“记忆力下降二年余，生活不能自理伴尿失禁二周”于入院。 患者二年前逐渐出现反应迟钝，少言寡语，不能识别家人，健忘等症状。此后病情缓慢进展，记忆力逐步下降，行动迟缓，行走需人搀扶。两周前，患者症状加重表现为计算能力进一步下降，近事记忆和远期记忆完全丧失，不能执行日常生活功能，以致生活不能自理，并出现尿失禁。患者病程中无头痛、头晕，无精神异常，无幻觉，无肢体抽搐，无发热，体重无明显下降。 2、既往史 既往有高血压病史十余年，血压最高为190/120 mm Hg，近期使用硝苯地平控释片、缬沙坦降压治疗；2型糖尿病六年，服用二甲双胍、拜唐萍控制血糖；五年前诊断为冠心病，目前服用阿司匹林、瑞舒伐他汀。10年前曾煤气中毒昏迷，无后遗症。曾患急性胰腺炎、阑尾炎，已愈。 3、体格检查 神清，体温T37℃，血压155/80 mm Hg，皮肤无皮疹及瘀点、瘀斑，心、肺、腹未见明显异常。少语，动作迟缓，计算力、近期记忆力、定向力下降。双侧瞳孔3 mm，等大等圆，对光灵敏，双侧眼球活动好，未见眼震。双侧鼻唇沟对称，伸舌居中，吞咽正常。颈软，无抵抗。四肢均能对称活动，肌力检查欠合作，四肢肌张力无明显增减，四肢腱反射对称正常，双侧病理征未引出。共济活动检查不配合。双下肢轻度水肿。 4、实验室检查 血常规：白细胞11×109／L，血红蛋白123 g/L，红细胞4．03×109／L，血小板101 ×109／L，中性细胞42．4％，淋巴细胞42．5％，单核细胞14．5％，嗜酸性细胞0．1％，嗜碱性细胞0，5％。 肝功能：ALT 37 U/L，AST 2I U/L，总胆红素14．1μmol/L，结合胆红素5．4μmol/L，总蛋白56 g/L，白蛋白31 g/L。 尿常规、粪常规、肾功能，电解质、凝血功能未见异常。 血氨：20 mmol/L。 肿瘤指标：CA125、CAl99、NSE、CEA、AFP、PSA、fPSA均正常。 风湿免疫指标：ANA，ENA，dsDNA、ANCA均正常。 脑脊液：压力正常。常规：白细胞20/μL(正常值：0-8／μL)，红细胞4/μL，潘氏(+)，生化：蛋白定量变944 mg/L(常值：150-450 mg/L)，糖2．49 mmol/L，氯化物119 mmol/L。 头颅CT提示脑室扩大、广泛脑白质病变、脑萎缩。 头颅MRI提示颅内多发缺血梗死灶，多发缺血脱髓鞘改变，双侧海马胼胝体萎缩，脑萎缩，左侧大脑中动脉局限性狭窄。 简易智能状态量表（MMSE）：7分，有认知功能障碍；Hachinski评分为7分；韦氏成人记忆及韦氏成人智力评定：患者无法配合。 二、诊疗经过 初步诊断：血管性痴呆可能性大；高血压病3级，极高危；2型糖尿病；冠状动脉粥样硬化性心脏病，心功能III级；左侧大脑中动脉局限性狭窄。 治疗经过：入院后继续硝苯地平控释片、缬沙坦控制血压，二甲双胍、拜唐萍控制血糖，肠溶阿司匹林抗血小板治疗，瑞舒伐他汀调脂、抗炎、稳定斑块。并予改善脑循环、营养神

老年痴呆的诊断和鉴别诊断

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痴呆病例分析 Document serial number【KK89K-LLS98YT-SS8CB-SSUT-SST108】

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