Diagnosing vascular cognitive impairment: Current challenges and future perspectives

You'll have to ask your doctor if vascular cognitive impairment is likely after stroke and what s/he is doing to prevent it.

Diagnosing vascular cognitive impairment: Current challenges and future perspectives

 

J Matthijs Biesbroek, Geert Jan Biessels

First Published January 30, 2022 Review Article 

https://doi.org/10.1177/17474930211073387

Article information

Abstract

Cerebrovascular disease is a major cause of cognitive decline and dementia. This is referred to as vascular cognitive impairment (VCI). Diagnosing VCI is important, among others to optimize treatment to prevent further vascular injury. This narrative review addresses challenges in current diagnostic approaches to VCI and potential future developments. First we summarize how diagnostic criteria for VCI evolved over time. We then highlight challenges in diagnosing VCI in clinical practice: assessment of severity of vascular brain injury on brain imaging is often imprecise and the relation between vascular lesion burden and cognitive functioning shows high intersubject variability. This can make it difficult to establish causality in individual patients. Moreover, because VCI is essentially an umbrella term, it lacks specificity on disease mechanisms, prognosis, and treatment. We see the need for a fundamentally different approach to diagnosing VCI, which should be more dimensional, including multimodal quantitative assessment of injury, with more accurate estimation of cognitive impact, and include biological definitions of disease that can support further development of targeted treatment. Recent developments in the field that can form the basis of such an approach are discussed.

Keywords

Vascular dementia, small vessels disease, diagnostic criteria, brain imaging

Introduction

Cerebrovascular disease is the second most common cause of dementia, after Alzheimer’s disease.^1,2 It is important to recognize and diagnose vascular contributions to cognitive impairment, among others to provide individualized treatment to prevent further vascular injury. This short review addresses diagnostic criteria for so-called “vascular cognitive impairment” (VCI). We will reflect on why it has proven difficult to capture VCI in a single diagnostic construct that informs on disease mechanisms, prognosis, and treatment; identify challenges in applying current VCI criteria in clinical practice; and discuss potential opportunities to update VCI criteria in light of recent developments in the field.

Evolution of diagnostic constructs

Vascular factors in dementia already featured prominently in early descriptions by Otto Binswanger and Alois Alzheimer at the turn of the 20th century, at that time largely based on neuropathology. The first formal diagnostic criteria for vascular contributions to cognitive impairment appeared some 30 years ago^3,4 and several iterations have appeared since.^1,2,5–7 Here we discuss these diagnostic constructs under the umbrella term VCI; acquired cognitive impairment attributed to cerebrovascular disease. Essentially, all VCI criteria entail three basic components: there should be acquired cognitive impairment, there should be cerebrovascular disease, and the two should be causally related. Yet, there are fundamental differences in how these components have been operationalized. Initial criteria only considered dementia,^3,4 an advanced stage of cognitive impairment where activities of daily life are affected. To accommodate the full spectrum of cognitive changes associated with vascular injury, also permitting diagnoses in earlier stages of disease, current VCI criteria encompass any degree of acquired cognitive impairment that can be objectified with cognitive testing.^5–7 All criteria are generally inclusive regarding types of cerebrovascular disease considered, including ischemic (both of arterial or venous origin) and hemorrhagic injury, large and small vessel disease, and considering emboli, vasculopathies, and hypoperfusion.^1,3,4,7 This inclusiveness clearly limits specificity in terms of disease mechanisms, but also in prognostic value and guidance for treatment. Where initial criteria aimed to capture “pure vascular dementia,” where no other pathologies explaining the cognitive deficit should be present,³ most criteria now acknowledge that cerebrovascular disease often co-occurs with other pathologies and that mixed pathologies need to be considered.^5–7 Indeed, mixed pathologies are the rule rather than an exception in people with cognitive impairment, particularly at older age.⁸ Even among patients assumed to have pure vascular dementia, a substantial subset also has biomarker evidence of co-occurring Alzheimer pathology.⁹ The third component of the diagnosis, attributing cognitive impairment to cerebrovascular disease, shows considerable variation between criteria. When there is a clear temporal relationship between the occurrence of one or multiple cerebrovascular events and the onset of impairment, causality may be self-evident. This may be even more clear if symptomatic lesions involve locations known to predispose to cognitive impairment, also referred to as strategic lesions.^5,10 However, the majority of people with cognitive impairment have so-called covert cerebrovascular disease, not manifested in a history of stroke. Because this covert disease is common also among older people without cognitive impairment, it has proven challenging to define the actual burden of vascular injury that can be accepted as cause of cognitive impairment. Finally, an emerging issue in VCI is that of cerebral reserve capacity: the functional impact of vascular injury is likely also determined by the resilience of the brain.¹¹ The latter is a construct that has proven difficult to operationalize and is not yet considered in diagnostic criteria.

Maybe we should take a step back and reflect on what the actual purpose of diagnostic criteria for VCI should be? Separate vascular etiologies from other non-vascular etiologies? In light of the common occurrence of mixed pathologies, this may be futile. Claim the biggest possible chunk of the “dementia causality pie”? The question is if this is a real service to the field, as “vascular” is not an etiological entity and heterogeneous in terms of mechanism and treatment. And are criteria primarily meant for clinical practice or for research, in particular clinical trials? Of note, the actual treatment of the vascular disease is generally not determined by its cognitive impact. Take, for example, a patient with a lacunar ischemic stroke without cognitive deficits, another patient with a strategic lacunar stroke in the left thalamus causing cognitive impairment, and another patient with pre-existent dementia due to Alzheimer’s disease with a lacunar stroke. Stroke prevention strategies would likely be the same in all cases. A final point to consider is that diagnostic criteria for VCI tend to categorize both cognitive impairment and vascular injury in terms of presence or absence. These dichotomizations may help to create a language for communication with patients and among professionals, but also tend to create biological and conceptual silos that do not match with reality.

More at link.