Vascular cognitive impairment

Linda A Hershey MD PhD (Dr. Hershey of the University of Oklahoma Health Sciences Center has no relevant financial relationships to disclose.)
Rhonda J Coleman-Jackson DNP APRN-CNS (

Dr. Coleman-Jackson of the University of Oklahoma Health Sciences Center in Oklahoma City has no relevant financial relationships to disclose.

Calin I Prodan MD (

Dr. Prodan of the University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center in Oklahoma City has no relevant financial relationships to disclose.

Howard S Kirshner MD, editor. (

Dr. Kirshner of Vanderbilt University School of Medicine received fees from Biogen for consulting work.

Originally released November 8, 1994; last updated December 8, 2020; expires December 8, 2023


Vascular cognitive impairment has superseded vascular dementia because of the limitations of the concept of vascular dementia.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 most common form of vascular cognitive impairment.


• Affected cognitive domains in vascular cognitive impairment typically include frontal and executive functions, attention, and speed of mental processing.


• Vascular cognitive impairment can coexist with Alzheimer disease and produce mixed dementia, which is the commonest form of all-cause dementia according to autopsy studies.


• There is good evidence that all these factors increase the risk of vascular dementia: age, lack of physical activity, obesity, midlife hypertension, diabetes, atrial fibrillation, and stroke.


• Modern practice concentrates on early detection of mild vascular cognitive impairment with a view to slowing of progression to dementia 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, subcortical small strokes, extensive subcortical white matter disease, and hemorrhage (Jellinger 2013).

Alzheimer disease versus vascular dementia. 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 accepted criteria for Alzheimer disease, 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. Some patients with vascular dementia, for example, experience a fluctuating cognitive course over several years, especially if recurrent ischemic events are prevented with antiplatelet and antihypertensive medications (Hershey et al 1986). These fluctuations occur whether the vascular dementia patients have small vessel disease, large vessel disease, or extensive subcortical white matter changes. 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 Hachinski ischemic scale (Table 1) (Hachinski et al 1975). Shorter forms of this scale have been evaluated using the Canadian Study of Health & Aging (Hachinski et al 2012).

Diagnostic criteria for vascular dementia. Early diagnostic criteria for vascular dementia defined dementia when there was both cognitive and functional impairment in instrumental activities of daily living (Hershey et al 1987a; Chui et al 1992; Roman et al 1993; Erkinjuntti et al 2000). These criteria identified medium to late cases of vascular cognitive impairment and thus underestimated the prevalence of all cognitive impairment due to vascular disease and denied 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), because this definition includes patients who have mild cognitive impairment (those who have memory or concentration problems but are still capable of managing instrumental activities of daily living). This is now widely accepted as a more appropriate concept than the old one of vascular dementia.

Vascular cognitive impairment criteria Image: Vascular cognitive impairment criteria
The most recent diagnostic criteria for mild and major VCI (vascular dementia) were outlined by a JACC Scientific Expert Panel (Iadecola et al 2019).

Infarct volume. The older concept of vascular dementia used to emphasize infarct volume (at least 50 ml of tissue loss) when describing single large infarcts or multiinfarct dementia (Roman et al 1993; Jellinger 2013). Now it is clear that cerebral microinfarcts and small subcortical infarcts are common causes of vascular dementia (van Veluw et al 2017; Iadecola et al 2019). Subsequent studies argued that infarct location or location of white matter change was also important. The importance of infarct location is illustrated by the thalamus, where small lesions can produce profound impairment.

Mixed dementia. 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 at autopsy 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 (Bowler et al 1998b; Holmes et al 1999; Lim et al 1999; Jellinger 2013). However, in cases meeting DSM-IV criteria for vascular dementia with prominent white matter hyperintensities on MRI, 69% showed no evidence of cerebral amyloid and may be “pure” cases of vascular dementia (Lee et al 2011). Among the first 50 patients with dementia in the Rush Memory and Aging Project who come to autopsy, 38% showed signs of both Alzheimer and vascular disease, 30% had pure Alzheimer disease, 12% had pure vascular dementia, and 12% had a combination of Alzheimer disease and Lewy body disease (Schneider et al 2007). Therefore, in this racially mixed group of dementia patients, mixed dementia was more prevalent than either pure Alzheimer disease or pure vascular dementia.

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.)



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




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