Clinicopathological validation study of four sets of clinical criteria for vascular dementia.

OBJECTIVE: The authors' goal was to validate the clinical criteria for vascular dementia of the State of California Alzheimer's Disease Diagnostic and Treatment Centers (ADDTC), the National Institute for Neurological Disorders and Stroke-Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN), DSM-IV, and ICD-10. METHOD: Sensitivity and specificity were assessed by comparing the clinical with the neuropathological diagnosis of 89 autopsied patients with dementia from a geriatric and psychiatric hospital. All cases were reviewed by a clinician and a neuropathologist who were blind to each other's findings. RESULTS: Neuropathologically there were 20 cases of vascular dementia, 23 cases of mixed dementia, and 46 cases of Alzheimer's disease among the autopsied patients. The sensitivity was 0.50 for DSM-IV criteria for vascular dementia, 0.70 for ADDTC criteria for possible vascular dementia, 0.55 for NINDS-AIREN criteria for possible vascular dementia, 0.20 for ICD-10 criteria for vascular dementia, 0.25 for ADDTC criteria for probable vascular dementia, and 0.20 for NINDS-AIREN criteria for probable vascular dementia. Specificity was 0.84, 0.78, 0.84, 0.94, 0.91, and 0.93, respectively. The proportion of cases clinically classified as vascular dementia ranged from 0% to 13% for neuropathologically confirmed cases of Alzheimer's disease and 9% to 39% for neuropathologically confirmed cases of mixed dementia. There was no statistically significant relationship between the neuropathological diagnosis and three of the clinical criteria sets studied (ICD-10 criteria for vascular dementia and ADDTC and NINDS-AIREN criteria for probable vascular dementia). CONCLUSIONS: Clinical criteria for vascular dementia are not interchangeable. The ADDTC criteria for possible vascular dementia are the most sensitive for the detection of vascular dementia; however, the DSM-IV criteria for vascular dementia and the NINDS-AIREN criteria for possible vascular dementia may be more effective in excluding mixed dementia. Given their inability to detect the vast majority of cases of vascular dementia, the ICD-10 criteria for vascular dementia and the ADDTC and NINDS-AIREN criteria for probable vascular dementia should be revised.     

Alzheimer's disease and brain infarcts in the elderly. Agreement with neuropathology

Clarifying the etiology of dementia is one of the most difficult diagnostic challenges, especially in the elderly. We examined the accuracy of clinical criteria to distinguish Alzheimer's disease (AD) and dementia associated with infarcts of the brain, either isolated (vascular dementia) or associated with degenerative lesions (mixed dementia). We carried out a prospective clinico-neuropathological study in a selected series of hospitalized patients. We evaluated the clinical aspects of 33 patients aged over 75 years by use of the criteria and scores of DSMIII, NINCDS-ADRDA, Loeb and Gandolfo, ADDTC and NINDS-AIREN and the Hachinski Ischemic Score. The neuropathological diagnosis was considered to be the gold standard. When comparing clinical criteria and neuropathology, the agreement was moderate for Hachinski's score (0.50) and Loeb's score (0.43) and substantial for the ADDTC (0.63) and the NINDS-AIREN (0.67). When mixed dementias were excluded, the agreement between all clinical criteria and scores and the pathological diagnosis rose to 0.88. Hachinski's score was the most sensitive (0.89) and the NINDS-AIREN the most specific (0.86) for the diagnosis of vascular dementia. In conclusion, all sets of clinical criteria distinguished pure AD from vascular dementia with a high accuracy whereas mixed dementia was clinically under-recognized. The NINDS-AIREN criteria were the most discriminating for the accurate identification of patients with mixed dementia. Received: 17 November 2001, Received in revised form: 14 May 2002, Accepted: 22 May 2002 Correspondence to Pr. Jean-Jacques Hauw     

Clinical diagnosis of dementia

This paper presents recommendations deriving from the Third Canadian Consensus Conference on the Diagnosis and Treatment of Dementia, concerning the clinical diagnosis of dementia. There are currently no universally accepted biological or radiological markers of dementia. In the absence of these, the diagnosis of dementia remains a clinical exercise aiming to integrate all available clinical and laboratory information. It is proposed that the currently used National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer’s Disease and Related Disorders Association (NINCDS/ADRA) criteria for diagnosis of Alzheimer’s disease (AD) be retained. The currently available vascular dementia (VaD) diagnostic criteria have variable accuracy. An integrative approach to VaD diagnosis based on all the available evidence (history, vascular risk factors, physical exam, clinical course, neuroimaging, cognitive impairment pattern) is recommended. The separation of Lewy body dementia (DLB) from Parkinson’s disease dementia (PDD) is based on the dominant clinical presenting feature of each syndrome, and relies on the duration of this feature: long duration of parkinsonian “motor” syndrome preceding dementia for PDD versus early/initial dementia accompanied by extrapyramidal symptoms for DLB. It is recognized that it is impossible clinically to characterize DLB with (pathologically) coexisting AD changes. The Frontotemporal group of dementia syndromes are discussed in regards to their typical clinical pictures, recognizing that their neuropathological substrate are not predictable from their mode of presentation. Finally, the particular rapid time sequence of evolution of the dementias due to prior disease is recognized as the clinically most useful distinguishing feature of these syndromes.     

Regulatory aspects of vascular dementia in the United States

There is significant interest in the development of new drugs to treat vascular dementia. However, before US approval of new drugs for this entity is possible, certain issues with regulatory implications need to be addressed. Is vascular dementia a distinct clinical syndrome with valid diagnostic criteria? Can this entity be distinguished from Alzheimer's disease (AD) and other causes of dementia? What design features are important for clinical trials in this disorder? The US Food and Drug Administration (FDA) convened a special meeting of the Peripheral and Central Nervous System Advisory Committee in an attempt to answer these questions. The conclusions from this meeting indicate that vascular dementia (VaD) is a pathologically heterogeneous disorder but appears to be reasonably distinguishable from AD dementia. The NINDS-AIREN diagnostic criteria are suitable as entry criteria for vascular dementia trials. Trials should be similar in duration to AD dementia trials and should employ a dual outcome strategy (cognitive + global/functional measures). For drugs that are believed to have a disease-modifying effect, clinical trials should study specific vascular dementia subtypes and would need to employ substantially different designs from those used currently. The term "vascular dementia" may not be entirely appropriate to describe this population.     

Vascular cognitive impairment

Cognitive impairment commonly accompanies clinical syndromes associated with vascular disease of the brain. Because of evolving definitional criteria, however, the frequency of cognitive impairment attributable to cerebrovascular disease is difficult to determine. Dementia occurs in up to one-third of elderly patients with stroke, a subset of whom have Alzheimer's disease (AD) rather than a pure vascular dementia syndrome. In fact, pure vascular dementia has been shown to be uncommon in most large autopsy series. A mixed etiology of AD and cerebrovascular disease is thought to become more common with increasing age, although no clinical criteria for the diagnosis of AD with cerebrovascular disease are currently available. Epidemiological studies have implicated subcortical small-vessel disease as a risk factor for cognitive impairment and dementia, but the cognitive expression and clinical significance of MRI white matter changes in individual patients is difficult to establish. The frequency of specific neuropathologic features of vascular cognitive impairment depends largely on study inclusion criteria. Cerebral meningocortical microangiopathies with distinctive clinicopathological profiles are associated with dementia in both sporadic cases and familial syndromes. In patients with AD, the contribution of amyloid-beta protein to the degree of cognitive impairment has not been clearly defined.     

Rethinking the dementia diagnoses in a population-based study: what is Alzheimer's disease and what is vascular dementia?. A study from the kungsholmen project

OBJECTIVE: To explore the hypothesis that older adults often are affected by more than one disease, making the differential diagnosis between Alzheimer's disease (AD) and vascular dementia (VaD) difficult. METHODS: Incident dementia cases (n = 308) from a population-based longitudinal study of people 75+ years were investigated. The DSM-III-R criteria were used for the clinical diagnosis of dementia. Data on vascular disorders (hypertension, cerebrovascular and ischemic heart diseases, heart failure, atrial fibrillation, diabetes) as well as type of onset/course of dementia were used retrospectively to reclassify dementias. RESULTS: Only 47% of the AD cases were reclassified as pure AD without any vascular disorder. Among subjects with AD and with a vascular component, cerebrovascular disease was the most common (41%). Only 25% of VaD were reclassified as pure VaD. Further, 26% of the pure AD subjects developed a vascular disorder in the following 3 years. CONCLUSIONS: Both vascular and degenerative mechanisms may often contribute to the expression of dementia among the elderly. Most of the AD cases have vascular involvements, and pure dementia types in very old subjects constitute only a minority of dementia cases.     

Vascular dementia: a diagnostic challenge

Although vascular dementia was described over a century ago, it remains a difficult and challenging diagnosis. Several sets of clinical criteria have been published in an effort to establish the presence or absence of vascular dementia in a standardized fashion. Clinical studies have demonstrated that they identify different groups of patients and are thus not interchangeable. Retrospective clinicopathological correlations have shown that most are insufficiently sensitive, although they are generally relatively specific. They accurately exclude pure Alzheimer's disease but may include 9% to 39% of mixed dementia cases (Alzheimer's disease and vascular dementia combined). Further studies are needed to develop better performing criteria that could lead to a broad consensus on the clinical diagnosis of vascular and mixed dementia.     

Defining dementia: clinical criteria for the diagnosis of vascular dementia

The recognition of cerebrovascular disease (CVD) as a contributing factor and a cause of dementia has led to the development of clinical criteria for vascular dementia (VaD). Due to high specificity, the consensus criteria developed by the National Institute for Neurological and Communicative Disorders and Stroke (NINDS)–Association Internationale pour la Recherche et l'Enseignement en Neurosciences (AIREN) have been used in controlled clinical trials to select patients with pure VaD. VaD is predominantly a subcortical frontal form of dementia with prominent executive dysfunction. In contrast, the criteria of the NINCDS–Alzheimer's Disease and Related Disorders Association (ADRDA) emphasize memory loss as the main feature to distinguish Alzheimer's disease (AD) from VaD and from other forms of dementia. Moreover, CVD may precipitate the clinical expression of AD. Although no criteria have been created specifically for patients having AD with CVD, the ischemic score, the Informant Questionnaire on Cognitive Decline in the Elderly and a history of prestroke mild cognitive impairment (MCI) may be useful for identifying patients with this mixed form of dementia.     

Vascular dementias

Cerebrovascular disorders are the second most frequent cause of dementia in late life next to Alzheimer's disease. A recent community-based autopsy study has demonstrated that relevant cerebrovascular changes are much more prevalent in individuals aged 70+ years than previously assumed. Furthermore, the combination between cerebrovascular lesions and Alzheimer-type pathology is the most common neuropathological finding in elderly patients with dementia. There is still some uncertainty about which types of cerebrovascular changes are most likely to cause cognitive impairment including dementia and which pathogenetic mechanisms are involved. Without doubt, however, the vascular dementias are a heterogeneous group of diseases in terms of etiology, histopathology, and clinical appearance. According to the vessel calibres and perfusion territories that are preferentially affected a distinction is commonly made between the frequent subcortical small-vessel disease and the rare cortical large-vessel disease. With these morphological subtypes three major clinical variants are associated: dementia due to subcortical lacunes and white matter changes including Binswanger's disease, multi-infarct-dementia, and dementia due to singular strategic infarcts. In most cases of dementia of cerebrovascular origin the pattern of intellectual impairment is frontal or subcortical, in contrast to the typical cortical presentation of Alzheimer's disease. Deterioration of executive function and attention as well as changes in personality, rather than memory loss, are the predominant symptoms. Therefore the current diagnostic criteria for dementia are poorly suited for the detection of vascular dementias. None of the criteria that have been specifically proposed for the diagnosis of vascular dementias provide clear guidelines for evaluating the causal relationship between cerebrovascular lesions and psychopathological findings. Further research will reveal whether clinical diagnosis can be improved by taking into account the heterogeneity of cerebrovascular diseases. A large proportion of dementias of cerebrovascular origin may be preventable by treating the risk-factors for stroke. Once significant cognitive impairment has occurred, however, there is no established pharmacological treatment for the vascular dementias to date. Only recently results of placebo-controlled clinical trials have become available showing that cholinergic treatment strategies are effective in vascular dementia and in dementia due to combined vascular and neurodegenerative pathologies.     

Role of functional brain imaging in the evaluation of vascular dementia

There are various types of underlying damage to tissue and vessels in vascular dementia, including (1) single or multiple infarcts that involve association and limbic cortices, (2) small subcortical infarcts disrupting cortico-subcortical circuits, and (3) white matter lesions. The clinical picture of vascular dementia varies, and the role of functional brain imaging of cerebral blood flow and metabolism would be expected to be different among subtypes of vascular dementia. The role and value of functional brain imaging is limited for cortical infarcts; it is very valuable in assessing the impact on cortical function for small subcortical infarcts; and it is probably useful for evaluating white matter lesions, but this needs to be determined in further studies. At least in research of vascular dementia, functional brain imaging criteria should be included for proper patient selection. Careful studies using functional imaging tools in a well-characterized patient population will be needed.     

A clinical role for 99mTc-HMPAO SPECT in the investigation of dementia?

OBJECTIVES—To provide the clinician with a guide to the clinical utility of ^99mTc-HMPAO single photon emission computed tomography (SPECT) and to the interpretation of specific test results in the differential diagnosis of dementia.
METHODS—Three hundred and sixty three patients with dementia were studied prospectively for a median three (range 1-6) years and classified into disease groups on the basis of established clinical criteria. The degree to which different patterns of cerebral blood flow (CBF) abnormality found on ^99mTc-HMPAO SPECT imaging at the time of initial patient presentation modified clinical diagnoses was determined by calculating the likelihood ratios for pairwise disease group comparisons. The optimal clinical usage of ^99mTc-HMPAO SPECT was determined by calculating the percentage of significant test results for each pairwise disease group comparison.
RESULTS—Bilateral posterior CBF abnormality was found to significantly increase the odds of a patient having Alzheimer''s disease as opposed to vascular dementia or frontotemporal dementia. Bilateral anterior CBF abnormality significantly increased the odds of a patient having frontotemporal dementia as opposed to Alzheimer''s disease, vascular dementia, or Lewy body disease. "Patchy" CBF changes significantly increased the odds of a patient having vascular dementia as opposed to Alzheimer''s disease. Unilateral anterior, unilateral anterior plus unilateral posterior, and generalised CBF abnormality failed to contribute to the differentiation of any of these forms of dementia.
CONCLUSIONS—^99mTc-HMPAO SPECT was found to be most useful in distinguishing Alzheimer''s disease from vascular dementia and fronto temporal dementia, and least useful in differentiating between Alzheimer''s disease and Lewy body disease, and between vascular dementia, frontotemporal dementia, and progressive aphasia. It is suggested that CBF SPECT should be used selectively and as an adjunct to clinical evaluation and CT.

     

Practice parameter: diagnosis of dementia (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology

OBJECTIVE: To update the 1994 practice parameter for the diagnosis of dementia in the elderly. BACKGROUND: The AAN previously published a practice parameter on dementia in 1994. New research and clinical developments warrant an update of some aspects of diagnosis. METHODS: Studies published in English from 1985 through 1999 were identified that addressed four questions: 1) Are the current criteria for the diagnosis of dementia reliable? 2) Are the current diagnostic criteria able to establish a diagnosis for the prevalent dementias in the elderly? 3) Do laboratory tests improve the accuracy of the clinical diagnosis of dementing illness? 4) What comorbidities should be evaluated in elderly patients undergoing an initial assessment for dementia? RECOMMENDATIONS: Based on evidence in the literature, the following recommendations are made. 1) The DSM-III-R definition of dementia is reliable and should be used (Guideline). 2) The National Institute of Neurologic, Communicative Disorders and Stroke--AD and Related Disorders Association (NINCDS-ADRDA) or the Diagnostic and Statistical Manual, 3rd edition, revised (DSM-IIIR) diagnostic criteria for AD and clinical criteria for Creutzfeldt--Jakob disease (CJD) have sufficient reliability and validity and should be used (Guideline). Diagnostic criteria for vascular dementia, dementia with Lewy bodies, and frontotemporal dementia may be of use in clinical practice (Option) but have imperfect reliability and validity. 3) Structural neuroimaging with either a noncontrast CT or MR scan in the initial evaluation of patients with dementia is appropriate. Because of insufficient data on validity, no other imaging procedure is recommended (Guideline). There are currently no genetic markers recommended for routine diagnostic purposes (Guideline). The CSF 14-3-3 protein is useful for confirming or rejecting the diagnosis of CJD (Guideline). 4) Screening for depression, B(12) deficiency, and hypothyroidism should be performed (Guideline). Screening for syphilis in patients with dementia is not justified unless clinical suspicion for neurosyphilis is present (Guideline). CONCLUSIONS: Diagnostic criteria for dementia have improved since the 1994 practice parameter. Further research is needed to improve clinical definitions of dementia and its subtypes, as well as to determine the utility of various instruments of neuroimaging, biomarkers, and genetic testing in increasing diagnostic accuracy.     

血管性痴呆国际诊断标准的解读与比较

在国外研究中比较常用的血管性痴呆诊断标准有多项。这些诊断标准对于痴呆、卒中以及痴呆和卒中的相关性有不同的定义,一些内容存在较大差异。临床病理对照研究显示这些血管性痴呆诊断标准的诊断敏感度均较低;部分临床诊断标准与病理诊断的一致性较差。目前常用的血管性痴呆国际诊断标准不能互换。     

Epidemiology: identifying vascular cognitive impairment

There has been a move in recent years to recognize that the most effective treatment for vascular dementia, and for the mixed component of mixed vascular dementia and Alzheimer's disease, lies not in treatment but in prevention. This requires that cases be identified before the onset of vascular damage (a stage termed "brain-at-risk") or, failing this, as soon as possible but certainly before dementia has developed. These early stages are termed vascular cognitive impairment (VCI). No criteria exist for this early stage of cognitive loss due to cerebrovascular disease and relatively little data exist to indicate how such cases might be identified. The data that do exist suggest that many of the traditional "vascular" features of sudden onset and stepwise progression, etc., are not common in VCI and new criteria will be needed to identify cases. This paper summarizes the data that describe the clinical, neuropsychological, and radiological features that are to be expected in VCI.     

Vascular Cognitive Impairment

Abstract: The term vascular cognitive impairment (VCI) is now employed to capture the spectrum of illness and disability arising from impaired cognitive function of vascular origin. As such, it supplants the more narrowly focussed terms "Vascular dementia (VaD)" and "multi-infarct dementia". It is meant to include both those whose cognitive impairment is different from that assumed by the usual criteria for dementia. Traditionally, dementia criteria have been modelled on AD, a disorder with more characteristic neuropathological and clinical disease expression than is seen in VaD, which can occur in many forms. VCI is common, and is associated with many adverse outcomes, including worse cognition, institutionalization, and death.
One form of VCI is coincident AD and VaD, a category which, although it has been comparatively neglected, may be amongst the most common forms of dementia. Another common form of VCI has a predilection for subcortical ischemic lesions, and for a clinical presentation which reflects frontal and subcortical involvement.
At present, there is no specific treatment for VCI, although several agents appear to offer the hope of both treatment and prevention. Further research on the clinical, pathological and mechanistic underpinnings of this important syndrome is needed. For a long time, VaD has been recognized as the second most common cause of dementia.^1,2) More recently, however, the concept of cognitive impairment in relation to cerebrovascular disease has been expanded. This paper will review the notion of "vascular cognitive impairment" (VCI) as it relates to clinical practice, and to our understanding of disease mechanisms in dementia and related disorders. It will propose that while the expanded concept has merit, within it are to be found distinct subgroups, including some of particular importance as targets for clinical trials of therapeutic and even preventive interventions.     

Diagnosis and management of vascular cognitive impairment and dementia

Vascular dementias (VaDs) are the second most common cause of dementia. Cerebrovascular disease (CVD) and stroke relates to high risk of cognitive impairment, but also relate to Alzheimer's disease (AD): Vascular cognitive impairment (VCI) and dementias extend beyond the traditional multi-infarct dementia. Pathophysiology of VaD incorporates interactions between vascular etiologies (CVD and vascular risk-factors), changes in the brain (infarcts, white matter lesions, atrophy), host factors (age, education) and cognition. Variation in defining the cognitive syndrome, in vascular etiologies, and allowable brain changes in current criteria have resulted in variable estimates of prevalence, of groups of subjects, and of the types and distribution of putative causal brain lesions. Should new criteria be developed? Ideally in constructing new criteria the diagnostic elements should be tested with prospective studies with clinical-pathological correlation: replace dogma with data. Meanwhile focus on more homogenous subtypes of VaD, and on imaging criteria could be a solution. Subcortical ischemic vascular disease and dementia (SIVD) incorporate small vessel disease as the chief vascular etiology, lacunar infarct and ischaemic white matter lesions as primary type of brain lesions, subcortical location as the primary location of lesions, and subcortical syndrome as the primary clinical manifestation. It incorporates two clinical entities "Binswanger's disease" and "the lacunar state". AD with VaD (mixed dementia) has been underestimated as a prevalent cause in the older population. In addition to simple co-existence, VaD and AD have closer interaction: several vascular risk factors and vascular brain changes relate to clinical manifestation of AD, and they share also common pathogenetic mechanisms. Vascular cognitive impairment (VCI) is a category aiming to replace the "Alzhemerized" dementia concept in the setting of CVD, and substitute it with a spectrum that includes subtle cognitive deficits of vascular origin, post-stroke dementia, and the complex group of the vascular dementias. As far there is no standard treatment for VaDs, and still little is known on the primary prevention (brain at risk for CVD) and secondary prevention (CVD brain at risk for VCI/VaD). There is no standard symptomatic treatment for VaD. Recently symptomatic cholinergic treatment has shown promise in AD with VaD, as well as probable VaD. Future focus should be directed to the distinct etiological and pathological factors: the vascular and the AD burden of the brain.     

Evaluation of 110 consecutive patients with dementias: a prospective study

We prospectively investigated 131 consecutive cases (both in- and outpatients) of suspected dementia to evaluate the relative frequency of different types of dementia in Chinese patients. Dementia was confirmed in 110 cases (84.0%). In contrast to the Western series, vascular dementia (39.1%) was slightly more frequent than the Alzheimer's disease (36.4%). Twelve cases (10.9%) of potentially treatable dementia were found. Careful clinical observation was the most useful part of the evaluation. CT scan of brain was the most useful laboratory test.     

Efficacy and adverse effects of cholinesterase inhibitors and memantine in vascular dementia: a meta-analysis of randomised controlled trials

BACKGROUND: Cholinesterase inhibitors and memantine do not have regulatory approval in most of the world for treatment of vascular dementia. A systematic review and meta-analysis was undertaken to assess the evidence for efficacy and safety of cholinesterase inhibitors and memantine in vascular dementia. METHODS: PubMed, BIOSIS, International Pharmaceutical Abstracts, and Cochrane registries were searched for randomised, placebo-controlled trials on cholinesterase inhibitors and memantine in patients with vascular dementia. Trial methods, clinical characteristics, outcomes, and adverse events were extracted and checked. Meta-analytic methods using fixed-effects models were used to give summaries of each drug's effects. FINDINGS: Three donepezil, two galantamine, one rivastigmine, and two memantine trials, comprising 3093 patients on the study drugs and 2090 patients on placebo, met the selection criteria. Trials were of 6-month duration with similar vascular dementia criteria and outcome measures. Cognitive effects on the Alzheimer's Disease Assessment scale were significant for all drugs, ranging from a -1.10 point mean difference (95% CI -2.15 to -0.05) for rivastigmine to -2.17 for 10 mg daily donepezil (95% CI -2.98 to -1.35). Only 5 mg daily donepezil had an effect on the Clinicians' Global Impression of Change scale (odds ratio 1.51 [95% CI 1.11-2.07]). No behavioural or functional benefits were observed, except for a -0.95 point difference (95% CI -1.74 to -0.16) with 10 mg daily donepezil on the Alzheimer's Disease Functional Assessment and Change Scale. Compared with placebo, more dropouts and adverse events (anorexia, nausea, vomiting, diarrhoea, and insomnia) occurred with the cholinesterase inhibitors, but not with memantine. INTERPRETATION: Cholinesterase inhibitors and memantine produce small benefits in cognition of uncertain clinical significance in patients with mild to moderate vascular dementia. Data are insufficient to support widespread use of these drugs in vascular dementia. Individual patient analyses are needed to identify subgroups of patients with vascular dementia who might benefit.     

Vaskuläre Demenz

The term vascular dementia refers to dementia syndromes which are caused by hypoxic-ischaemic brain lesions. Lesions found in vascular dementia such as complete and incomplete infarctions, selective necroses, and others are nonspecific. The characteristics and severity of the clinical syndrome are determined by the size and topography of the ischaemic lesions. Among others, age and pre-existing brain atrophy are risk factors for the development of dementia based on vascular lesions. There is a high comorbidity of Alzheimer's disease and vascular dementia. It can be presumed that ischaemic lesions and Alzheimer-like pathological changes exert additive effects in the manifestation of the clinical dementia syndrome. The diagnostic process follows three steps: 1. presence of a dementia syndrome, 2. presence of cerebrovascular disease, 3. evidence for a relationship between 1 and 2. Present diagnostic criteria, such as "International Classification of Diseases" (ICD-10), "National Institute of Neurological Disorders," "Stroke-Associated Internationale pour la Reserche et l'Enseignement en Neurosciences" (NINDS-AIREN), and "Alzheimer's Disease Diagnostic and Treatment Centers" (ADDTC) describe differing constellations and show little congruence. Estimates of the prevalence depend highly on the set of criteria used. Hence, they differ considerably.     

Memory failure in binswanger's disease and alzheimer's disease

The heterogeneity within vascular dementia has made neuropsychological research in this area difficult to interpret. We studied a subtype of vascular dementia, Binswanger's disease (BD), diagnosed according to recently specified clinical and radiological criteria. Measures of episodic and semantic memory were administered to BD patients, patients with Alzheimer's disease (AD) comparable to the BD sample in dementia severity, age, and education, and normal controls. Episodic memory was more defective in AD than in BD; these patient groups were equally impaired on measures of semantic memory. The findings suggest that assessment of episodic memory may be useful in differentiating AD from BD.