CONSEQUENCES OF STROKE

Vascular cognitive impairment (VCI)

David Goldemund M.D.
Updated on 28/08/2024, published on 15/12/2023

cerebral vascular disease can lead to the development of cognitive deficit (VCI) or vascular dementia (VaD), and it also influences the course of other dementias (such as Alzheimer’s dementia)

Definition

Vascular Cognitive Impairment (VCI) is a term used to describe a range of cognitive deficits resulting from cerebrovascular disease or other conditions that affect cerebral blood vessels
it is currently preferred over vascular dementia (VaD) because classic criteria for dementia may not be present for a long time
- classic criteria involve a global and progressive cognitive decline in one or more cognitive domains and noticeable interference with daily life
the key features include:
- cerebrovascular disease – VCI is primarily associated with damage to the brain’s blood vessels, often due to conditions like stroke, small vessel disease, or other vascular disorders
- heterogenous cognitive deficits
  - a wide range of cognitive changes that can vary in severity, from mild cognitive impairment (MCI) to more severe forms of cognitive impairment, including those meeting the criteria for dementia
  - deficits occur in various domains, including memory, executive function, attention, language, and visuospatial skills
- course – VCI lacks a consistent clinical presentation and course (unlike, for example, Alzheimer´s disease)
  - deficits may progress over time and lead to the development of vascular dementia
- presence of traditional vascular risk factors
early detection and management of vascular risk factors are crucial for reducing the incidence and progression of VCI

Epidemiology

VCI is one of the most common types of cognitive impairment, second only to Alzheimer’s disease (AD)
the prevalence and incidence vary by geographic region and population (ethnicity, genetics); VCI is believed to be underdiagnosed, and it often coexists with other forms of dementia, such as Alzheimer’s disease. This can make it challenging to estimate its true prevalence accurately
- advanced diagnostic techniques, such as neuroimaging and CSF analysis, may help in distinguishing VCI from other forms of dementia
it is more common in older adults
the risk of dementia in patients after stroke is 5-fold compared to the healthy population of the same age
- individuals with a history of multiple strokes are at highest risk
patients have a lower 5-year survival rate compared to the healthy population (39% versus 75%)
- cardiovascular and cerebrovascular diseases are the leading cause of premature death

Risk factors

traditional cardiovascular risk factors
most significant are:
- age
- diabetes mellitus
- undiagnosed or poorly controlled arterial hypertension
- hypercholesterolemia
- smoking
- atrial fibrillation
- a history of cerebrovascular events

Classification of VCI

different classifications often use different designations for the same clinical entities

Location

Etiology

Course

Cortical

strategically located isolated infarct
multiple territorial strokes

Subcortical

multiple lacunar strokes → Binswanger disease
white matter lesions (WMLs)

Combination of cortical and subcortical lesions

Ischemic

hemorrhagic

acute (<3 months after stroke)

subacute-chronic

Strategically located isolated infarct

cognitive, mnestic, and behavioral changes that typically do not meet the general criteria for dementia (global and progressive impairment)
often, it involves a so-called isolated cognitive deficit
- aphasia
- apraxia
- gnostic disorders
- dysexecutive syndrome
there is typically a sudden onset following a stroke

Strategically localized infarction in the temporal lobe causing a severe amnestic syndrome

Strategic infarction in the PCA territory causing impaired speech fluency, neglect syndrome, apraxia, and alexia

Perforators	so-called thalamic dementia
ACA	loss of motivation and initiative emotional lability disinhibition
MCA	dominant hemisphere aphasic disorders Gerstmann’s syndrome (finger agnosia, right-left disorientation, agraphia, and acalculia) non-dominant hemisphere neglect syndrome (non-dominant hemisphere) visual-spatial agnosia with spatial orientation disorder constructional apraxia
PCA	amnestic syndrome (mediobasal areas of the temporal lobe, thalamus, fornix) visual disorders in terms of hemianopia various forms of visual agnosia prosopagnosia with right/left bilateral involvement of the temporooccipital cortex color recognition agnosia with left ventromedial occipital lobe lesion

Multiple territorial or lacunar infarcts

“multi-infarct dementia”
sudden onset of difficulties
stepwise deterioration of cognitive function following ischemic attacks

Multiinfarct impairment in a patient with Moya-moya

Subcortical vascular impairment

it usually develops due to damage to arterioles in the subcortical area (small vessel disease)
a chronic course, with gradual stepwise deterioration and fluctuations
multiple lacunar infarcts and/or damage to the white matter (white matter lesions – WML) on MRI (can be quantified using FAZEKAS or ARWMC scales)
clinically, it primarily manifests as executive function impairment, retrieval deficits, and psychomotor slowing
common objective findings include quadripyramidal syndrome, pseudobulbar syndrome, gait disturbances, incontinence, psychiatric symptoms, and more.
this category typically includes conditions such as Binswanger’s disease or genetic small vessel diseases (such as CADASIL)

Diagnostic evaluation

Neuroimaging

brain CT or better MRI + vascular imaging with a demonstration of relevant vascular damage

Clinical evaluation

to distinguish AD, a color perception test (Ishihara charts) could help – in AD, color perception is impaired
- sensitivity of 80.6%, a specificity of 87.5% for a cut-off value of 32.5 [Arnaoutglou, 2017]

Psychological evaluation and tests

the purpose of any screening is to roughly differentiate between normal and pathological conditions; the results may be further refined through specialized neuropsychological testing
in practice, the most commonly used screening tool is the Mini-Mental State Examination (MMSE)
- It is a brief and relatively easy-to-evaluate test, but it is important to ensure that it is administered correctly
- when used alone, it has limited diagnostic value regarding the nature of cognitive deficit
- It is not sensitive to executive function impairments (which are common in VCI) – It is advisable to include at least the Clock Drawing Test (CDT)
during specialized examinations, it is important to consider the patient’s current capabilities and the increased fatigue of cognitively impaired patients. Adjust the testing duration and the selection of tests accordingly

Examples of neuropsychological testing methods suitable for detecting cognitive function decline
Intellect (global status)	Wechsler Intelligence Tests (WAIS-R, or WAIS-III)
Memory	Wechsler Memory Scale (WMS-III) Rey-Osterrieth Complex Figure
Executive abilities	Trail Making Test – Part B Stroop Test Cognitive Estimation Test Wisconsin Card Sorting Test
Language	Verbal Fluency Tests Token Test alternatively, Western Aphasia Battery
Visuospatial and constructional abilities	Rey-Osterrieth Complex Figure Clock Drawing Test (CDT) Blocks and Puzzles from WAIS-R
Psychomotor speed	Symbols from WAIS-R Trail Making Test – Part A
Attention	Trail Making Test – Part A Repeating Numbers from WAIS-R
Symbolic abilities	Reading, counting, writing + drawing a person
Emotionality and depression	Beck Depression Inventory
Behavior	Instrumental Activity of Daily Living Neuropsychiatric Inventory Neurobehavioral Rating Scale

Diagnostic criteria

Pitfalls of existing criteria

diagnostic criteria for vascular dementia were based on the model of cognitive changes in Alzheimer’s disease (AD), with dominant damage to the hippocampus and, therefore, memory. However, vascular disease can lead to widespread cognitive deficits, while memory may remain intact
the course may not be a distinguishing factor either – not all vascular cognitive deficits progress in a stepwise manner. For example, subcortical ischemic disease has a course that is more similar to AD, but clinically, it is characterized by a predominance of executive dysfunction rather than memory impairment
it is questionable whether it is even possible to create universally applicable diagnostic criteria for a condition with a broad etiopathogenic basis and diverse clinical presentations
some experts, therefore, prefer to create diagnostic criteria for individual subtypes of VCI (see, for example, the diagnostic criteria for subcortical ischemic disease proposed by Erkinjuntti)

Hachinski ischemic score (HIS)

Hachinski Ischemic Score (HIS)

a simple and easy-to-use tool used since 1974 for a rough differentiation between multiinfarct dementia and Alzheimer’s dementia, but it is not suitable for distinguishing mixed forms
a higher score is generally indicative of a higher likelihood of vascular dementia
- 0-4 points – suggestive of Alzheimer’s dementia
- 7 or more – suggestive of Vascular Dementia (VaD)

abrupt onset of dementia	1
stepwise progression of dementia	1
fluctuating cognitive symptoms (symptoms vary in severity from day to day)	1
nocturnal confusion	1
relative preservation of personality despite cognitive impairment	0
emotional incontinence (outbursts or tearfulness)	1
gait disturbance	1
history of one or more strokes	1
hypertension	1
evidence of multi-infarct dementia on CT or MRI	1

NINDS-AIREN criteria

these criteria were created specifically for research purposes (highly specific, but with low sensitivity)
to establish a diagnosis of probable VCI according to the NINDS-AIREN criteria, three fundamental conditions must be met:
- presence of cognitive deficit – defined as a decline in memory and two or more other cognitive abilities.
- existence of corresponding cerebrovascular brain damage (on imaging methods):
  - multiple territorial infarcts or hemorrhages
  - strategically located single infarct.
  - extensive white matter involvement
  - multiple lacunar infarcts in the basal ganglia and white matter
- causal relationship between the two above-mentioned conditions:
  - for example, the onset of cognitive deficit within 3 months after a recognized stroke
  - sudden deterioration of cognitive functions or gradual progression of cognitive deficit with progressive findings on imaging examinations
definitive (certain) diagnosis of vascular dementia is established when the criteria for probable vascular dementia are met, there is histopathological evidence of cerebrovascular brain disease (from biopsy or autopsy), and other causes of dementia have been ruled out.
on the other hand, the vascular etiology is questioned in cases of early onset and progressive worsening of memory deficits and other cognitive abilities in the absence of corresponding lesions on CT or MR

NINDS-AIREN Diagnostic Criteria

I. Possible

cognitive syndrome + objective findings, but lacking clear temporal relationship or imaging evidence of cerebrovascular disease
evidence of cerebrovascular disease; however, the cognitive deficit has unclear onset or fluctuating course

II. Probable

dementia + cerebrovascular disease + their clear association

III. Definite – histopathological evidence

Classification of Subcortical Ischemic Vascular Dementia/Disease (SIVD)

I. Cognitive deficit
- executive dysfunction
- memory impairments (especially retrieval difficulties)
II. Cerebrovascular disease (CVD)
- typical CT or MRI findings (see table)
- neurological deficit
  - “frontal” gait, pyramidal, and pseudobulbar syndrome
onset between 44-75 years
history of arterial hypertension, diabetes (often subclinical)
progression over 5-10 years

CT/MRI criteria of SIVD

extensive white matter involvement:
- lesions > 10 mm in size
- diffuse confluent hyperintensity (> 25 mm)
multiple lacunar infarcts (> 5) in subcortical gray matter and lacunar infarcts in white matter
absence of cortical infarctions/hemorrhages

Subkortical Ischemic Vascular Disease (SIVD)

Management

early detection is crucial as it can help in managing underlying conditions and potentially slow or stop the progression of cognitive decline

Causal therapy of cerebrovascular disease

→ Stroke prevention

Symptomatic therapy

Cholinesterase Inhibitors and NMDA Antagonists

studies have demonstrated the effectiveness of cholinesterase inhibitors and NMDA receptor antagonists
- donepezil, galantamine, rivastigmine
- memantine
they slow the progression of cognitive deficit, have a positive effect on behavioral and psychological symptoms of dementia (depression, anxiety, etc.), and on the performance of daily activities

Treatment of associated depression → poststroke depression

Other medications

the effect of other drugs (e.g., nootropics, extracts from ginkgo biloba) has not been convincingly demonstrated by studies, but it cannot be ruled out

Cognitive training, psychotherapy, rehabilitation, caregiver support, diet → Stroke rehabilitation

training tailored to the specific deficits that the individual patient is experiencing
a diet rich in fish, seafood, vegetables, citrus fruits, and olive oil, as well as a diet high in folic acid, vitamins B6 and B12, and antioxidants

FAQs

What is vascular cognitive impairment?

a cognitive decline that ranges from mild cognitive impairment to more severe dementia
primarily caused by vascular problems (atherosclerosis, arteriolopathy, etc.) that alter blood flow and lead to brain damage (ischemia or hemorrhage)

What are the symptoms of vascular cognitive impairment?

symptoms vary but often include difficulties with problem-solving, focusing, organizing thoughts, and memory
changes in mood, such as depression, and physical symptoms, like difficulty walking, can also occur

What is the difference between vascular dementia and vascular cognitive impairment?

vascular dementia is a more severe form of VCI; while VCI can range from mild to severe, vascular dementia specifically refers to cases where cognitive impairment is global and interferes with daily living

How is vascular cognitive impairment diagnosed?

diagnosis involves a medical history review, neurological exams, cognitive tests, and brain imaging studies

Is vascular cognitive impairment the same as Alzheimer's disease?

No, they are different. Alzheimer’s is primarily caused by neurodegenerative processes, while VCI is due to blood flow issues in the brain. However, symptoms can overlap, and a person can have both conditions.

Can vascular cognitive impairment be treated?

treatment focuses on managing the underlying vascular conditions, slowing progression, and alleviating symptoms
this includes controlling vascular risk factors (blood pressure, cholesterol levels, lifestyle changes like diet, exercise, etc.)

How important is early detection of vascular cognitive impairment?

early detection is crucial as it allows for early treatment of underlying conditions and potentially slows the progression of cognitive decline