Natural history of dementia associated with lacunar infarctions

doi:10.1016/S0022-510X(02)00261-7

Journal of the Neurological Sciences

Volumes 203–204, 15 November 2002, Pages 53-55

https://doi.org/10.1016/S0022-510X(02)00261-7 Get rights and content

Abstract

Background: Lacunar stroke (VaD-L) is the most common stroke subtype associated with vascular dementia (VaD). Objective: To evaluate the rate of cognitive and behavioral changes in patients with probable VaD-L. Methods: We measured rates of change on the Mini-Mental State Examination (MMSE), Digit Span, Logical Memory, Controlled Oral Word Association Test, CERAD battery and the Neuropsychiatric Inventory (NPI) of 77 [age at entry 65.9±8.1 (mean±standard deviation) years] patients with probable VaD, periventricular white matter and basal ganglia lacunae, longitudinally studied for 25.7±11 months. Results: Mean number of follow-up visits was 2.6. Overall annual vascular event rate was 0.25. VaD-L in mildly and moderately impaired patients is characterized by progressive cognitive and behavioral decline. The rate of cognitive and behavioral progression depends on the occurrence of vascular episodes (VE) during the course of the illness [(−1.1) MMSE and (+4.0) NPI points annually without VE vs. (−2.0) and (+10.3) points following VE]. The rates of progression are a function of the severity of the cognitive and behavioral impairment. Impaired cognition is associated with impaired behavior. A subgroup of VaD-L patients runs a progressively deteriorating course despite the absence of clinically apparent new vascular episodes. Conclusion: VaD-L is characterized by cognitive and behavioral decline in 83% of the patients. The rate of decline is determined mainly by the severity of the cognitive and behavioral impairment at baseline and by the occurrence of new vascular episodes.

Introduction

The most common stroke subtype associated with vascular dementia (VaD) is the lacunar stroke (VaD-L) [1]. Most lacunae are located in the basal ganglia and in the cerebral white matter [2]. Clinically, the dementia associated with subcortical lacunar infarction is characterized by slowing of information processing, memory deficit, impaired executive functions, and gait dysfunction. These are frequently accompanied by personality and mood alterations. To the best of our knowledge, the rate of decline of VaD-L has not been described to date.

Our aim in the present study was to characterize the course and progression of patients clinically diagnosed with VaD-L.

Section snippets

Methods

Patients were recruited from among referrals to a Cognitive Neurology Unit in Haifa, Israel. Patients with previous clinical history of neurological, psychiatric, somatic, or toxic causes for dementia were excluded. Evaluation included general physical and neurological assessment, calculation of the Hachinski Ischemia Score (HIS) [3], the Mini-Mental Status Examination (MMSE) [4], Digit Span and Logical Memory subscales of the Wechsler Memory Test—Revised; Controlled Oral Word Association Test,

Results

Seventy-seven patients (53 men and 24 women; mean age 65. 9±8.1 years), with mild to moderate dementia (MMSE 24±4.3) participated in the study. Mean length of follow-up was 25.7±11 months (7.1±59.7, median 25.5 months) during which 206 evaluation visits, reflecting 129 BVI, were performed. New vascular events occurring following the first visit were reported in 33 patients (41 BVI). Vascular event rate was 0.25. MMSE scores of 83.11% of patients deteriorated, and of 16.88% remained unchanged or

Discussion

We describe the rate of progression of patients with VaD-L the course of which was punctuated by additional cerebrovascular and cardiovascular episodes but not by large vessel infarctions. VaD-L in mildly and moderately impaired patients is characterized by a progressive cognitive and behavioral deterioration. The course may be gradual, steady, and/or fluctuating, but the final outcome is one of deterioration. In the advent of a vascular episode, deterioration is steeper. Memory, especially

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The most frequent causes of cognitive impairment and dementia of vascular origin are multi-infarct encephalopathy, lacunar status, vascular leukoencephalopathy, infarcts in strategic regions, hippocampal sclerosis, and infarcts in watershed areas. Several lesions often converge in the same individual (Hachinski et al., 1974; Hauw, 1995; Román, 2000; Vinters et al., 2000; Aharon-Peretz et al., 2002; Szirmai et al., 2002; Norrving, 2003; Kalaria et al., 2004a; Reed et al., 2004; Rossi et al., 2004; Gold et al., 2005; Kalimo and Kalaria, 2005; Jicha et al., 2006; Pantoni et al., 2006; Probst et al., 2007; Hauw et al., 2008; Jellinger, 2008; Ferrer, 2010, 2015). The vascular diseases most commonly linked to cognitive impairment and dementia of vascular origin are small blood vessel disease and atherosclerosis (Thal et al., 2012).
The chapter describes the epidemiology of cerebrovascular diseases, anatomy of the cerebral blood vessels, pathophysiology of ischemia, hypoxia, hypoxemia, anemic hypoxia, histotoxic hypoxia, carbon monoxide damage, hyperoxid brain damage and decompression sickness, and selective cell and regional vulnerability; diseases of the blood vessels including atherosclerosis, hypertensive angiopathy, small vessel disease, inflammatory vascular diseases, cerebral amyloid angiopathies, CADASIL, CARASIL and other diseases that can lead to cerebrovascular occlusion; intracranial and intraspinal aneurysms and vascular malformations; hematologic disorders that can cause cerebral infarct or hemorrhage; brain ischemic damage; and spontaneous intracranial bleeding. Within ischemic brain damage, focal cerebral ischemia, hemorrhagic infarct, brain edema, penumbra, global cerebral ischemia, venous thrombosis, lacunas and lacunar state, status cribosus, granular atrophy of the cerebral cortex, hippocampal sclerosis, vascular leukoencephalopathy Binswanger type and multi-infarct encephalopathy are discussed in detail. Cognitive impairment of vascular origin deserves an individual section.
Cognitive dysfunction in stroke survivors: A community-based prospective study from Kolkata, India
2013, Journal of Stroke and Cerebrovascular Diseases
The frequency of cognitive dysfunction among community stroke survivors (SS) is not known in India. This prospective study investigated the prevalence of poststroke mild cognitive impairment (psMCI) and poststroke dementia (psDem), the annual progression rate to dementia, and pertinent risk factors in a sample population of SS in Kolkata, India between September 2006 and July 2010. From a community-based stroke registry, 281 SS were assessed at baseline year after excluding attrition due to various causes. Validated cognitive tools were applied by trained field workers under supervision of a neuropsychologist. The assessment was repeated annually for consecutive three years. The mean follow-up period was 1.89 years (range, 1-3 years). The period prevalence rate of psDem was 13.88% (95% confidence interval [CI], 9.91%-18.90%) at baseline, and the average annual progression rate to dementia was 3.53% (95% CI, 2.09%-5.58%). Compared with subjects without dementia, those with psDem were significantly older at first-ever stroke and more likely to have cortical atrophy. The period prevalence rate of psMCI was 6.05% (95% CI, 1.45%-13.64%) at baseline, and 10.6% (95% CI, 4.57%-20.88%) of these subjects converted to psDem annually. Survival analysis of psDem patients showed a greater risk of death in psDem SS as compared to nondemented SS (hazard ratio, 2.65; 95% CI, 1.72-6.15). Our data suggest that the overall prevalence of psDem is higher than that of psMCI, possibly related to nonexclusion of prestroke dementia, but that the average annual progression rate of SS to psDem and that of psMCI to psDem are comparable. Older age at first-ever stroke and cortical atrophy are associated with increased risk for dementia among SS.
Vascular dementia
2012, Journal of the Neurological Sciences
Citation Excerpt :
This slower progression is also seen in placebo arms of drug studies in VaD patients [62–64], although the measures used may not be equally sensitive to measure decrease in VaD and in AD. VaD natural history is type-specific and depends on brain preconditions For instance, the occurrence of an ischemic stroke increases the risk of developing dementia significantly [65,66]. Pre-stroke cognitive impairment increases this risk of a more severe cognitive impairment immediately after the stroke [66] .
The epidemic growth of dementia causes great concern for the society. It is customary to consider Alzheimer's disease (AD) as the most common cause of dementia, followed by vascular dementia (VaD). This dichotomous view of a neurodegenerative disease as opposed to brain damage caused by extrinsic factors led to separate lines of research in these two entities. Indeed, accumulated data suggest that the two disorders have additive effects and probably interact; however it is still unknown to what degree. Furthermore, epidemiological studies have shown "vascular" risk factors to be associated with AD. Therefore, a clear distinction between AD and VaD cannot be made in most cases, and is furthermore unhelpful. In the absence of efficacious treatment for the neurodegenerative process, special attention must be given to the vascular component, even in patients with presumed mixed pathology. Symptomatic treatment of VaD and AD is similar, although the former is less effective. For prevention of dementia it is important to treat all factors aggressively, even in stroke survivors who do not show evidence of cognitive decline. In this review, we will give a clinical and pathological picture of the processes leading to VaD and discuss its interaction with AD.
Cognitive impairment of vascular origin: Neuropathology of cognitive impairment of vascular origin
2010, Journal of the Neurological Sciences
Citation Excerpt :
Isolated lacunae have been considered as a rare cause of cognitive impairment [8,46]. Yet the presence of lacunae in strategic sites or the combination of lacunae with other lesions such as diffuse lesions of the white matter is a proven substrate of cognitive impairment and dementia [47–51]. Binswanger's disease is the paradigm of vascular leukoencephalopathy and it is characterized by demyelination and axonal loss in the white matter of the cerebral hemispheres affecting the occipital lobes, the temporal lobe, the parietal and the frontal lobes, but sparing the subcortical U-fibers (Fig. 4).
The term cognitive impairment of vascular origin is used to designate global cognitive deficits as well as focal neurological deficits such as aphasia, apraxia and agnosia of vascular/circulatory origin. It has been useful for identifying early clinical and neuroradiological alterations that might permit therapeutic strategies geared to curbing the progression of cerebrovascular disease. Multi-infarct encephalopathy, infarcts in strategic areas, lacunae and lacunar status, Binswanger's encephalopathy, hippocampal sclerosis, cortical granular atrophy and watershed infarcts are common lesions. Hypertension and vascular diseases such as arteriosclerosis, small blood vessel disease, inflammatory diseases of the blood vessels, Sneddon syndrome, cerebral amyloid angiopathies, cerebral autosomic dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), and Maeda's syndrome are causative of cognitive impairment of vascular origin. Other less common causes are hereditary endotheliopathy with retinopathy, neuropathy and strokes (HERNS), cerebro-retinian vasculopathy (CRV), hereditary vascular retinopathy (HVR) (all three linked to 3p21.1–p21.3), hereditary infantile hemiparesis with arteriolar retinopathy and leukoencephalopathy (HIHRATL) (not linked to 3p21), fibromuscular dysplasia, and moya-moya disease. Lack of uniformity of clinical manifestations, the variety of vascular diseases and circulatory factors, the diverse, but often convergent, neuropathological substrates, and the common association with unrelated neurodegenerative diseases in the elderly, make it hard to assume a single clinical approach in the diagnosis and treatment of cognitive impairment of vascular origin. Rather, environmental and genetic risk factors, underlying vascular diseases, associated systemic, metabolic and neurodegenerative diseases and identification of extent and distribution of lesions with morphological and functional neuroimaging methods should be applied in every individual patient.
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The presence of such norms facilitates appropriate comparison; newly evaluated community residents can be compared with other community residents of comparable age, race/ethnicity, and education; patients at tertiary medical care centers can be compared with other patients at the same types of centers. The CERAD neuropsychology battery (sometimes in whole, sometimes in part), has been used with various groups who, in addition to those listed in Tables 2 to 4, include Native Americans [53], older Israelis (in Hebrew) [54,55], elderly in Colombia [56,57], and older persons in India, China, Southeast Asia, Latin America and the Caribbean, and Africa [58,59]. The clinical battery has been referenced as a standard by several clinical studies that indicate that they used NINCDS/ADRDA and CERAD criteria for AD.
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Natural history of dementia associated with lacunar infarctions

Abstract

Introduction

Section snippets

Methods

Results

Discussion

J. Psychiatr. Res.

Characterization of risk factors for vascular dementia: the Honolulu–Asia Aging Study

Neurology

Vascular dementia: diagnostic criteria for research studies. Report of the NINDS-AIREN International Workshop

Neurology