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  • Updated 11.07.2023
  • Released 11.08.1994
  • Expires For CME 11.07.2026

Vascular cognitive impairment



Vascular cognitive impairment has superseded vascular dementia because of the limitations of the concept of vascular dementia.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 patients with vascular cognitive impairment include executive function, processing speed, attention, and verbal fluency.

• 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. Patients with mixed dementia can experience an accelerated decline on measures of working memory, processing speed, and verbal memory.

• There is good evidence that all these factors increase the risk of vascular dementia: age, lack of physical activity, obesity, midlife hypertension, high cholesterol, cigarette smoking, diabetes, atrial fibrillation, atrial cardiomyopathy, stroke, and post-stroke seizures. Vascular health and white matter microstructural integrity are better maintained in those who have resilience factors, such as higher education and occupational level, and good blood pressure control.

• 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 (27; 36). 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 (49).

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 (44). These fluctuations occur whether the patients with vascular dementia 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) (39). Shorter forms of this scale have been evaluated using the Canadian Study of Health & Aging (37).

Diagnostic criteria for vascular dementia. Early diagnostic criteria for vascular dementia defined dementia as when there was evidence of both cognitive and functional impairment in instrumental activities of daily living (42; 14; 91; 23). 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 (38), 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. The Cognitive Classification Consensus Study recommended the term “mild VCI” to refer to the mild cognitive impairment stage of vascular cognitive impairment and “major VCI” to refer to the vascular dementia stage (103).

Vascular cognitive impairment criteria
This figure illustrates the concept of vascular cognitive impairment that relates to severity. (Contributed by Dr. John Bowler.)

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 (91; 49). Now it is clear that cerebral microinfarcts and small subcortical infarcts are common causes of vascular dementia (119; 47; 24). Subsequent studies have argued that infarct location or the location of white matter change was also important (52). The importance of infarct location is illustrated by the thalamus, where small lesions can produce profound cognitive 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 (98; 49; 06; 29). 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 (61). 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 (98). Therefore, in this racially mixed group of dementia patients, mixed dementia was more prevalent than either pure Alzheimer disease or pure vascular dementia. When cognitively normal members of the 1946 British Birth Cohort were followed with MRI and amyloid-PET at the mean age of 71, they had signs of both amyloid pathology (plaques) and vascular pathology (white matter hyperintensities) (56). This study suggested that these effects were distinct and additive.

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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