Vascular cognitive impairment (VCI), is a common yet complex group of disorders caused by impacts to the brain’s blood vessels. This collection of conditions is second only to Alzheimer’s disease in prevalence among dementias and is particularly important for clinical neuropsychologists, as neuropsychological assessment remains pivotal in diagnosis, monitoring, rehabilitation and care planning.
Vascular Cognitive Impairment and Dementia #
The term “vascular dementia” has traditionally been used to describe significant cognitive decline resulting from cerebrovascular disease, but this terminology is increasingly seen as too narrow and potentially misleading. “Vascular cognitive impairment” (VCI) is now preferred, as it more accurately captures the full spectrum of cognitive difficulties caused by vascular pathology in the brain. While “vascular dementia” implies a relatively late stage, where cognitive deficits are severe enough to substantially impair daily functioning, many individuals affected by cerebrovascular changes experience milder deficits that do not meet the clinical threshold for dementia. The concept of VCI encompasses both these milder forms and more advanced cases, reflecting the continuum of vascular-related cognitive dysfunction. Adopting the term “vascular cognitive impairment” thus encourages earlier recognition, diagnosis, and intervention, and acknowledges the heterogeneity and complexity of these conditions beyond the binary presence or absence of dementia.
Vascular Pathologies Underlying Dementia #
Several different types of vascular damage can lead to cognitive decline:
- Large vessel infarcts (cortical and subcortical strokes): Major strokes affecting large arteries can cause sudden, focal deficits.
- Small vessel disease: Chronic, progressive damage to the brain’s small vessels leads to “watershed” infarcts and white matter changes, resulting in gradual cognitive decline; this is a leading cause of subcortical vascular dementia.
- Strategic infarcts: Even a single, small stroke in an area crucial for cognition (e.g., thalamus, angular gyrus) may cause sudden-onset dementia or prominent symptoms.
- Microbleeds and haemorrhages: Cerebral amyloid angiopathy and hypertension can result in small bleeds, affecting networks critical to cognition.
- Hypoperfusion: Persistent low blood flow due to heart failure or severe hypotension can cause global white matter injury.
- Mixed pathology: Most commonly in advanced age, vascular brain changes co-occur with neurodegenerative (e.g., Alzheimer’s) pathology.
Clinical Presentation: Signs and Symptoms #
The clinical manifestations of vascular cognitive impairment are shaped by the type, location, and extent of vascular damage. For the neuropsychologist, it is critical to appreciate this variability, as well as the typical cognitive profile and associated neurological or psychiatric features.
Pattern of Cognitive Deficits in Vascular Cognitive Impairment #
The vascular cognitive impairment profile typically differs from that of typical Alzheimer’s disease in that VCI tends to be skewed towards executive and subcortical deficits, often with less initial memory impairment:
- Executive dysfunction: Problems with planning, sequencing, set-shifting, working memory, inhibition, and mental flexibility are hallmark features. These appear as difficulty organising tasks, multitasking, or adapting to new situations.
- Attention and processing speed: Cognitive slowing (bradyphrenia) and impaired complex attention are early and prominent. Patients may seem mentally sluggish, require more time to respond, and struggle to sustain focus or switch between tasks.
- Memory: While memory may be affected, deficits typically centre on retrieval and inefficiency rather than the rapid forgetting seen in Alzheimer’s. Recognition memory is often better preserved, and cueing helps recall (often not present in Alzheimer’s).
- Visuospatial and constructional skills: These vary but can be impaired, particularly with extensive white matter involvement.
- Language: Usually preserved, but “dysexecutive” language symptoms (circumlocution, reduced verbal fluency) and motor speech issues (dysarthria) may be seen if subcortical structures are involved.
Behavioural and Psychiatric Features #
- Apathy: Loss of motivation and flattened affect are frequent and can be mistaken for depressive disorders.
- Depression: Late-onset depression is common and can worsen cognitive outcomes.
- Emotional lability: Patients may experience inappropriate or exaggerated emotional responses (pseudobulbar affect).
- Disinhibition and irritability in some cases.
Neurological and Physical Signs #
- Focal neurological deficits: Unlike in Alzheimer’s, patients may have observable neurological signs such as hemiparesis, gait disturbance, visual field deficits, or dysphagia, particularly in cases following stroke.
- Gait and motor issues: “Lower body parkinsonism” (shuffling gait, falls, slowed movement) is typical in subcortical small vessel disease.
- Urinary incontinence may also develop in advanced cases with frontal-subcortical involvement.
Course and Progression #
- Stepwise decline: Cognitive deterioration after distinct cerebrovascular events (e.g., stroke) with intervening periods of relative stability.
- Gradual progression: More typical of small vessel disease and leukoaraiosis, in which white matter changes accumulate slowly, with insidious cognitive and functional changes.
- Fluctuations: Some patients experience fluctuating alertness, particularly if there is comorbid delirium or underlying multi-infarct pathology.
Neuropsychological Assessment and Differential Diagnosis #
The Neuropsychologist’s Role in Vascular Cognitive Impairment #
Clinical neuropsychologists play a central part in:
- Early detection: Sensitive measures can reveal subtle deficits before clear everyday impairment is observed.
- Diagnostic clarification: Careful neuropsychological profiling helps distinguish vascular from Alzheimer’s and other dementias, especially when imaging and clinical history are ambiguous.
- Measuring functional impact: Determining whether cognitive impairments interfere with everyday life and thus meet criteria for dementia.
- Monitoring change: Tracking cognitive trajectories informs prognosis and intervention and can highlight progressive decline, plateau, or improvement with risk factor management.
- Family and patient education: Clarifying the nature of impairments and recommending compensatory strategies.
Key Differential Diagnoses #
- Alzheimer’s disease: Prominent episodic memory impairment with rapid forgetting, less executive dysfunction initially, slow gradual progression.
- Dementia with Lewy bodies: Features prominent fluctuations, visual hallucinations, Parkinsonian features, and sometimes REM sleep behaviour disorder.
- Normal pressure hydrocephalus: Triad of gait disturbance, urinary incontinence, and cognitive impairment resembling subcortical VCI.
- Frontotemporal dementias: Behavioural changes or language disturbances, usually with less prominent vascular risk history.
- Pseudodementia (depression-induced cognitive impairment): Mood history, variable effort, and improvement with treatment differentiate these cases.
Diagnostic Criteria and Brain Imaging in Vascular Cognitive Impairment #
While neuropsychological findings are key, diagnosis of vascular cognitive impairment or vascular dementia generally requires evidence of significant cerebrovascular disease (on MRI or CT) and a temporal link between vascular events and cognitive decline. Common diagnostic systems include the NINDS-AIREN criteria and DSM-5 definitions for major or mild vascular neurocognitive disorder. For reference however, below is a real world case shared from Radiopaedia demonstrating brain imaging for vascular abnormalities.
An “almost certain” diagnosis of vascular dementia © Radiopaedia
Practical Considerations for Clinical Neuropsychologists #
- Account for motor and sensory deficits in assessment selection (e.g., avoid timed, motorically demanding tasks in patients with hemiparesis).
- Assess insight and functional impact: Some individuals retain insight (especially in subcortical/vascular profiles) but may present with more emotional distress.
- Collaborate in multidisciplinary teams: Work closely with neurologists, geriatricians, and allied health professionals for holistic management, including risk factor reduction.
- Management focus: There are few drug therapies with proven benefit; optimal care centres on aggressive management of vascular risk factors (blood pressure, cholesterol, diabetes), psychosocial support, and education for families and carers.
Conclusion #
Vascular dementia comprises a diverse group of cognitive disorders caused by various forms of cerebrovascular injury. Clinical neuropsychologists are uniquely positioned to characterise cognitive profiles, contribute to differential diagnosis, monitor progression, and support patients and families. Recognition of the critical role vascular factors play in cognitive health re-emphasises the need for early identification, comprehensive assessment, and multidisciplinary management of both the cognitive and medical aspects of care.
Presentation on Vascular Cognitive Impairment / Vascular Dementia #
© Prof Alan Thomas Newcastle University
Neuropsychological Assessment for Vascular Cognitive Impairment #
If you or a loved one is experiencing cognitive difficulties similar to those mentioned above, do please contact us for neuropsychological assessment from a clinical neuropsychologist.
