Vascular cognitive impairment

John V Bowler MD (Dr. Bowler of the Royal Free Hospital and University College Medical School in London has no relevant financial relationships to disclose.)
Vladimir C Hachinski MD (Dr. Hachinski of the University of Western Ontario has no relevant financial relationships to disclose.)
Martin R Farlow MD, editor. (

Dr. Farlow of Indiana University received research grant support from Accera, Biogen, Eisai,  Eli Lilly, Genentech, Roche, Lundbeck, Chase Pharmaceuticals, Novartis, Suven Life Sciences Ltd, and Boehringer Ingelheim; honorariums from Eisai, Forest Laboratories, Pfizer, Eli Lilly and Company and Novartis for speaking engagements; and fees from Accera, Alltech, Avanir, Axovant, Biogen, Eisai Med Res, Inc., Eli Lilly and Company, FORUM Pharmaceuticals, Genentech, Inc., Grifols, Helicon, INC Research, Lundbeck, Medavante, Medivation, Merck, Neurotrope Biosciences, Novartis, Pfizer, Prana, QR Pharm., Riovant Sciences Inc., Roche, Sanofi-Aventis, Schering-Plough, Toyama Pharm, Stemedica Cell Technologies Inc., vTv Therapeutics and UCB Pharma for consultancy. His spouse was employed by Eli Lilly.

)
Originally released November 8, 1994; last updated July 11, 2016; expires July 11, 2019

This article includes discussion of vascular cognitive impairment and vascular dementia. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Vascular cognitive impairment has superseded vascular dementia because of the limitations of the concept of vascular dementia. In this article, the conceptual basis of vascular cognitive impairment is reviewed along with a critique of the old criteria for vascular dementia. Also reviewed are developments in the management of vascular cognitive impairment, in which there have been advances in both slowing disease progression and in symptomatic relief.

Key points

 

Subcortical vascular cognitive impairment due to small vessel cerebrovascular disease is the commonest form of vascular cognitive impairment.

 

• Affected domains typically include frontal and executive functions.

 

• Vascular cognitive impairment commonly coexists with Alzheimer disease and produces mixed dementia, which is the commonest form of dementia.

 

Multi-infarct dementia is rare.

 

• Modern practice concentrates on early detection with a view to the prevention of progression wherever possible.

Historical note and terminology

Despite the recognition of both Alzheimer disease and a form of vascular dementia (Binswanger disease) at the end of the 19th century, for most of the 20th century dementia was routinely attributed to arteriosclerosis and consequent chronic cerebral ischemia. This view changed with the near simultaneous recognition that many cases of dementia were Alzheimer disease and the demonstration that infarcts and not chronic ischemia were the basis of what came to be termed multi-infarct dementia (Fisher et al 1968; Hachinski et al 1974). Cerebral blood flow and metabolism studies later confirmed the absence of chronic cerebral ischemia. Instead, they showed a modest fall in cerebral blood flow in vascular dementia, which is accompanied by a normal oxygen extraction ratio. Thus, cerebral blood flow is matched to decreased metabolic demands. The term “vascular dementia” subsequently replaced multi-infarct dementia because it was recognized that there were many etiologies apart from multiple infarcts including single infarcts in eloquent areas, episodes of hypotension, leukoaraiosis, incomplete infarction, and hemorrhage.

However, by the 1980s, Alzheimer disease was increasingly recognized and came to overshadow vascular dementia to the extent that some authors asserted that multi-infarct dementia was rare. Because of the predominance of Alzheimer disease and the presence of criteria, these criteria came to form the basis for those of vascular dementia. This basis for the definition resulted in early criteria for vascular dementia emphasizing memory loss and usually the progression and irreversibility of cognitive decline, none of which are necessarily the case. Alzheimer disease was separated from vascular dementia using clinical features thought to reflect vascular risk factors, vascular events, and the manifestations of systemic and cerebral vascular disease. These elements are typically codified using the ischemic score (Table 1) (Hachinski et al 1975).

Early criteria for vascular dementia also defined dementia as the level of cognitive impairment at which normal daily functions are impaired. They will therefore identify only late cases, so underestimating the prevalence of cognitive impairment due to vascular disease and denying early cases the benefit of early preventative treatment. To avoid this there has been a paradigm shift towards a new concept, that of vascular cognitive impairment (VCI) (Hachinski and Bowler 1993), and this is now widely accepted as a more appropriate concept than the old concept of vascular dementia.

Image: Vascular cognitive impairment criteria
However, validated criteria for vascular cognitive impairment are still awaited. Development of these will require alternative rating scales and screening tools that focus on the cognitive domains most affected in vascular disease.

The older concept used to emphasize infarct volume, but this is simplistic because of the importance of location. The importance of infarct location is illustrated by the thalamus, where small lesions can produce profound impairment. There has been debate over the minimum volume of infarction needed to produce dementia, but this is a matter of limited significance given the importance of infarct location. Early work implicated volumes over 20 mL and, in particular, over 50 mL, but modern work has found smaller volumes, usually in the range of 1 to 30 mL, to be significant. The importance of site means that the correlation between infarct volume and neuropsychological deficit is poor when all stroke types are studied together. Within any 1 location the correlation between infarct volume and cognition improves, as would be expected as the effect of location is minimized. Because of the importance of site, it is extremely unlikely that there exists a volume of infarction that can reliably predict vascular cognitive impairment, other than at meaninglessly large volumes.

A further major change has been the increasing recognition of mixed dementia, where vascular cognitive impairment coexists with other causes of dementia, particularly Alzheimer disease. This is now known to be common. Eighty percent of the elderly in the United Kingdom have evidence of cerebrovascular disease (Neuropathology Group of the Medical Research Council Cognitive Function and Ageing Study (MRC CFAS) 2001) and mixed vascular cognitive impairment, and Alzheimer disease may account for up to half of all dementia (Snowdon et al 1997; Bowler et al 1998b; Holmes et al 1999; Lim et al 1999). However, in cases meeting DSM-IV criteria for vascular dementia with prominent leukoaraiosis, 69% show no evidence of cerebral amyloid and may be “pure” cases (Lee et al 2011). Furthermore, the interaction between the vascular component and other components more than doubles the rate of progression when compared to pure Alzheimer disease alone (Snowdon et al 1997; Heyman et al 1998).

Table 1. The Ischemic Scale

(Scores over 7 suggest a vascular etiology for dementia, whereas scores of 4 or less do not support a vascular etiology.)

Value

 

Abrupt onset
Stepwise deterioration
Fluctuating course
Nocturnal confusion
Relative preservation of personality
Depression
Somatic complaints
Emotional incontinence
History/presence of hypertension
History of strokes
Evidence of associated atherosclerosis
Focal neurologic symptoms
Focal neurologic signs

___2
___1
___2
___1
___1
___1
___1
___1
___1
___2
___1
___2
___2

TOTAL SCORE

___

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