Neuropsychology and Vascular Cognitive Impairment and Dementia

Synopsis:

Neuropsychology is an integral component of healthcare assessment for persons with vascular contributions to cognitive impairment and dementia. Since syndromes of vascular cognitive decline have multiple and varying pathophysiologies, anatomical brain locations, and levels of severity, neuropsychological assessment can be critical to clarify the cognitive manifestations of the disease, potential consequences for the patient and family, as well as the prognosis for future life planning. Cognitive profiles of vascular cognitive declines and relevant neuropsychological literature are reviewed here to provide the practicing physician with guidance for best clinical care practices.

Introduction

Vascular cognitive impairment and dementia (VCID) is an umbrella term that encompasses the entire spectrum of cognitive disorders that result from cerebrovascular disease (CVD), ranging from mild vascular cognitive impairment (VCI) to fully developed vascular dementia (VaD) as well as multiple types of mixed dementia. Several review articles have described VCID in the context of cerebral small vessel disease, asymptomatic carotid stenosis, stroke, and heart disease, recognizing that not only large strokes but also smaller, subtler vascular dysfunction can affect cognition¹. Recent estimates have identified VCID as the second most common type of dementia after Alzheimer’s disease (AD), and the most common mixed dementia, being a contributing factor in about 70% of dementia cases^2,3. Some recent neuropathological data even suggest that so-called pure cases of AD are comparatively rare². A more contemporary view suggests that cerebrovascular dysfunction and other degenerative pathology are most likely interdependent, with each potentiating and/or inducing the other.

Despite its high prevalence, VCID remains underdiagnosed. While neuroimaging has vastly improved the ability to detect cerebrovascular injuries that impair cognition, the mere presence of CVD is not sufficient to diagnose vascular dementia. In fact, community-based studies have identified vascular pathology in more than 75% of older adults, and as much as one third to one half of older adults have chronic macroscopic infarcts³. Clinical features, such as focal neurological signs and/or cognitive screening, are often used in conjunction with neuroimaging to inform clinical suspicions for VCID. However, accurate diagnosis of VCID can be challenging for many reasons, including that: (1) VCID is often observed in patients with no history of clinical stroke, (2) post-stroke cognitive declines may be related to other types of brain disorders (e.g., Alzheimer’s disease [AD] and forms of Lewy Body), (3) Cognitive screening tools (e.g., MMSE and MOCA) typically demonstrate only moderate sensitivity in the detection of cognitive decline (i.e., > 30% of cognitively impaired patients produce a normal result)^4,5, and (4) individual differences in factors such as depression and cognitive reserve can notably influence the effects of CVD on manifest cognitive impairment.

Further complicating matters, diagnostic criteria for VCID have been revised numerous times (>16) since Hachinski’s proposed terminology of multi-infarct dementia in 1974⁶. Consequently, progress in understanding and management of vascular cognitive impairment (VCI) has been hampered by lack of consensus on diagnosis, reflecting the use of multiple different assessment protocols. Given these various complicating factors, the value of neuropsychology consultation in cases of suspected vascular dementia can be particularly high. In fact, a recent critical review of the incremental value of neuropsychological assessment concluded that it could improve diagnostic classification, enhance accuracy of long-term daily-life prognosis across the lifespan, and advance healthcare decision making leading to cost savings⁷.

Subtypes of Vascular Cognitive Impairment and Dementia

Because VCID can vary markedly in its cognitive presentation, it can be helpful to understand the various etiological subtypes of the disorder, although there can often be considerable overlap among them⁸. Subtypes of VCID are continually evolving as we acquire knowledge of the impact of vascular abnormalities in the cerebrum. The underlying pathophysiology can involve chronic hypoperfusion, endothelial dysfunction, blood-brain barrier disruption, and, in the case of microbleeds, bleeding-prone vessel pathology. Though many like to subtype VCID using inspection of the MRI lesions, the cause, size or location is not directly associated with specific cognitive, behavioral or functional outcomes in many cases. There are diverse vascular mechanisms leading to cognitive decline.

Ischemic vascular dementia is the most common subtype, resulting from lack of oxygen to parenchyma due to blockages, or narrowing, of the brain’s arteries. Cerebral small vessel disease (SVD) affects the brain’s smaller arteries, leading to more diffuse and widespread lesions, including white matter hyperintensities (WMHs), leukoaraiosis, lacunar infarcts, and microbleeds. These processes contribute to the complex clinical presentations seen in patients with cerebral small vessel disease (SVD). These manifestations of SVD often occur together due to shared risk factors and underlying mechanisms. However, each can also occur independently, reflecting the heterogeneity of small vessel disease. The simultaneous presence of lacunes, microbleeds, subcortical small vessel infarcts, and WMHs in a patient indicates a more extensive burden of SVD. Stroke typically occurs from large vessel disease, or restricted oxygen due to obstruction of large arteries.

VCID resulting from multiple cerebral infarctions has been historically recognized as “multi-infarct dementia”, which is commonly associated with post-stroke cerebral volume loss and can present in a stepwise progression of cognitive decline that is temporally concurrent to each subsequent event. By contrast, VCID can also occur following a single strategic infarct, whereby the pattern of neuropsychological deficits is dependent on the area of impact. For example, strategic infarct within certain regions the basal ganglia can disrupt critical prefrontal-subcortical circuits involved in executive and motor functioning, infarcts in the left angular gyrus can result in characteristic symptoms of Gerstmann’s syndrome, and posterior circulation strokes can produce significant memory problems that can mimic Alzheimer’s disease.

Hemorrhagic vascular dementia occurs due to bleeding within or around the brain, often from the rupture of weakened blood vessels. Hemorrhagic strokes generally have lower incidence than ischemic events, but they are nonetheless associated with cognitive impairment and may in fact render higher risk for VCID when they do occur⁹. Hemorrhagic bleeds can result from hypertension since chronic high blood pressure can weaken blood vessel walls. Cerebral amyloid angiopathy is a condition where amyloid protein deposits weaken the blood vessels in the brain and increase the risk of hemorrhage. While MRI data can inform the clinical approach to management, most VCID clinical approaches benefit from addressing modifiable risk factors (See Box 1)^10–12. There are also nonmodifiable risk factors including genetics, older age, female gender, and non-White ethnicity¹².

Box 1: Modifiable Risk Factors:

• Cardiovascular Diseases: Conditions that affect the heart and blood vessels, such as heart disease and atherosclerosis, significantly increase the risk.

• Hypertension: High blood pressure is a leading risk factor, contributing to the narrowing and blockage of arteries that supply the brain.

• Diabetes: Diabetes mellitus increases the risk of vascular dementia by contributing to blood vessel damage throughout the body, including those supplying the brain.

• High Cholesterol: Elevated levels of LDL cholesterol can lead to atherosclerosis, which narrows and blocks arteries, reducing blood flow to the brain.

• Smoking: Smoking contributes to vascular problems and increases the risk of vascular dementia.

• Obesity: Excess body weight is associated with vascular problems and diabetes, which are risk factors for vascular dementia.

• Physical Inactivity: A sedentary lifestyle is a risk factor for cardiovascular diseases and subsequently vascular dementia.

• Poor Diet: Diets high in saturated fats, trans fats, and cholesterol can contribute to vascular health problems.

• Excessive Alcohol Use: Heavy drinking can damage blood vessels and increase the risk of vascular dementia.

Lastly, genetic vasculopathies encompass a group of inherited conditions that affect the blood vessels, leading to an increased risk of vascular disease, including stroke, aneurysms, and other vascular abnormalities. These disorders can impact both large and small vessels and vary widely in their clinical presentation, depending on the specific genetic mutation and the type of vessels involved. Given the vast number of genetic contributions to VCID and VaD, it is critical to obtain a comprehensive family history and refer for genetic testing when indications of cognitive declines are suspected or evident in relatives.

Neuropsychology referrals in vascular patients

The decision as to whether and when to refer to neuropsychology can depend on various factors, notwithstanding the availability and integration of neuropsychology services within a given clinical setting. While the presence of CVD in non-demented older adults is common and may not be grounds for a referral in and of itself, it is clear that higher CVD burden is associated with greater risk for vascular-related cognitive impairment. The presence of extensive WMHs (>1SD above the group mean) is associated with a more than doubling of risk of VCID in older adults^13–14. In a longitudinal study, upwards of 60% of patients with small vessel disease at baseline went on develop VCID within 3–5 years¹⁵. Thus, the presence of high CVD burden among older adult patients is often sufficient to warrant a neuropsychology referral, particularly in the context of subjective- and/or proxy- reported cognitive concerns. To this end, routine inquiry about cognitive difficulties in daily life can help elicit potential areas of subjective concern. Reported problems with attention, problem-solving, and executive dysfunction may be especially salient clues about underlying VCID.

The need for neuropsychological referral may still be called for in the absence of reported cognitive complaints, and it is noted that anosognosia is often a prominent feature in many forms of dementia. The presence of other risk factors for VCID can heighten suspicion for the disorder and inform need for neuropsychology referral. Such risk factors include advanced age, presence of multiple cardiovascular risk factors, ApoE e4 genotype (associated with cerebral amyloid angiopathy), and familial history of stroke and/or VCID. Several longitudinal studies have also consistently reported a deleterious effect of midlife hypertension on later life cognitive function^16–17.

Cognitive screening tools (e.g., MoCA, MMSE) and functional rating scales (e.g., Modified Rankin scale, Barthel Index) can be useful tools that may be feasibly administered across diverse clinical settings. In this regard, the Montreal Cognitive Assessment (MoCA) has in some cases been reported to be superior to the Mini-Mental State Exam (MMSE) for VCID, presumably due to its greater emphasis on executive function, though this is not a consistent finding¹⁸. Regardless of approach, most cognitive screeners are fairly insensitive to slowed processing speed, visual memory, and right-hemisphere lesions. Moreover, consensus on the appropriate cut-off scores for impairment can vary markedly. Overall, cognitive screeners typically show modest sensitivity in detecting cognitive decline, and significant findings can sometimes be affected by other, noncognitive factors (e.g., reported functional limitations could be explained by physical limitations and/or cultural expectations). Thus, they do not always suffice for diagnostic purposes in and of themselves, although they may be helpful in determining need for neuropsychological referral. Ultimately, the value of neuropsychology for the detection and tracking of VCID remains the preferred standard.

Certainly, clinical evidence of a recent stroke or repeated TIAs can prompt neuropsychology referral. In these instances, however, the timing of the referral can impact the outcomes of the evaluation. For example, neuropsychological evaluation immediately post-stroke is helpful to make immediate decisions about independence in activities of daily living, though significant changes typically continue to occur over time and may warrant periodic re-evaluation. The best time for neuropsychology referral depends on the referral question. Some examples of common referral questions are shown in Box 2.

Box 2: Neuropsychology referral questions.

1. What is the severity and cognitive pattern of consequences from a most recent stroke or transient ischemic attack?

2. What is the profile of cognitive impairments in this patient with mild cognitive decline, high amyloid biomarker levels, and evidence of mild vascular anomalies on MRI?

3. What is the rate of cognitive change over time in this patient with (e.g., chronic hypertension, partial seizures, headaches, transient ischemic attacks, stroke(s), and how does this profile contribute to prognosis?

4. What diagnosis is most consistent with the neuropsychological pattern in this patient with cognitive complaints?

5. How do the patient’s cognitive deficits impact their daily functioning? What level of care or additional treatment considerations might they require based on the observed cognitive deficits?

In addition to its diagnostic value, neuropsychological referral can be useful even when the diagnosis of VCID is already present. Neuropsychological findings used for strategic planning of educational, occupational, or functional capacity, in an effort to maximize one’s highest levels of capacity while maintaining low levels of frustration, error, or distress is typically of universal value. Though performance-based validation of vascular and apoptotic findings on MRI is typically reported, neuropsychology is no longer used as a primary method for lesion localization. Rather, ecological validity of subjective- or proxy-reported concerns can be demonstrated and treatment plans can be devised with direct knowledge of specific cognitive strengths, weaknesses, and progression or stability⁷. In some instances, neuropsychological evaluation can be used to determine driving and decision-making capacity, though it is often helpful to state these concerns explicitly in the referral question to ensure appropriate testing is included accordingly.

From a practical standpoint, there are some scenarios in which neuropsychological referral may not be appropriate or feasible. For example, patients with more advanced dementia, substantial impairment on cognitive screeners (e.g., MoCA <10/30), and/or post-stroke delirium likely will not benefit from testing, as the tasks will likely be too challenging to detect a specific cognitive profile. In some (but not all) circumstances, meaningful cooperation in neuropsychological testing can also be hampered by severe depression, behavioral alterations, severe aphasia, and/or significant sensory problems. Proactively addressing modifiable and/or reversible contributions to cognitive decline (e.g., untreated sleep apnea, poorly managed diabetes, vitamin deficiencies) can help remove additional confounds that can cloud diagnostic accuracy in cognitive assessment.

Neuropsychology presentations of VCID

Neuropsychological presentations of VCID can be quite varied, reflecting the diverse nature of the vascular pathologies that underlie the condition. In early stages of VCID, the most commonly reported symptoms include deficits in executive functions, attention, and processing speed. This is consistent with distribution patterns of VCID pathology that more strongly affect frontal and parietal lobes within periventricular white matter, resulting in greater disruption of frontal-subcortical circuitry. Unlike Alzheimer’s disease, which typically begins with memory impairment, vascular dementia may start with different cognitive deficits depending on the areas of the brain that are affected. More than five systematic reviews with meta-analyses have been conducted to differentiate Alzheimer’s disease (AD) from vascular dementia (VaD), most recently of 122 studies (total patient sample size >23,000)¹⁹. With increasing methodological rigor, conclusions show strong support for better performance of patients with VaD on memory tests as well as evidence for better performance of AD patients on some tests of executive functioning. While confirming the differential cognitive profiles documented for over two decades, reports also validate the significant overlap in the scores of most tests, further supporting recent disease models of shared pathophysiology and emphasizing the complexities between vascular and degenerative contributions to dementia. The information presented in the following section is a summary of the key neuropsychological features commonly observed within each cognitive domain among individuals with VCID and/or VaD.

Executive Dysfunction

• Predominant Feature: The most characteristic impairment in VaD is executive dysfunction. This includes difficulties with planning, organizing, problem-solving, setting priorities, and multitasking. Patients with VCID often show impairments on EF tasks of abstraction, mental flexibility, reasoning, and working memory.

• Processing Speed: Slowed cognitive processing speed is commonly observed, which affects the ability to perform tasks quickly and efficiently. Among patients with heavy WMH burden, reduced processing speed is often the most common cognitive finding²⁰.

Learning and Memory

• Memory Retrieval: Unlike the profound memory storage deficits seen in Alzheimer’s, memory issues in VaD often involve retrieval difficulties. Thus, spontaneous recall of information may be limited, but individuals may show improvement with cuing and/or relatively preserved recognition memory.

• Impact of Executive Dysfunction: Memory problems may be exacerbated by executive dysfunction, as difficulties with organizing thoughts can impair the ability to recall information. Other dysexecutive features in memory function may include instances of source memory confusion, perseveration, and difficulty with single trial learning that improves with repetition and/or added structure/organization.

Attention and Concentration

• Declines in attention and concentration can have an early onset in VCID. Because attentional capacities are central to so many daily tasks, deficits in this domain can have downstream effects impacting various other aspects of cognitive functioning. As a result, subjective complaints in other domains can sometimes be better explained by attentional problems. For example, difficulty with attention can impact one’s ability to learn new information, and thus may be subjectively reported as a primary memory difficulty.

Language

• Variable Impact: Language abilities can be affected, especially if the left hemisphere is involved, but the pattern is less consistent than in Alzheimer’s disease. Problems may include difficulty finding words (anomia) or issues with fluency, particularly in phonemic/letter fluency^9,21.

• Communication: In some cases, individuals might have trouble following complex conversations or instructions due to impaired processing speed and attention.

Visuospatial Abilities

• Depending on Affected Areas: Impairments in visuospatial skills, such as difficulty judging distance or recognizing objects and faces, can occur, especially if the right hemisphere or parietal lobes are affected.

Intellectual Functioning

• Fluid Reasoning: Problem-solving and reasoning skills typically show earliest decline in VaD, while more crystallized knowledge tests of intellect may be relatively spared.

Mood and Personality Changes

• Mood-related difficulties are common and can have a strong influence over functional outcomes and quality of life over and above cognitive problems alone²².

• Depression and Anxiety: High rates of depression and anxiety are seen in individuals with VaD, which can be related both to neuropsychiatric effects of lesions themselves as well as psychological adjustment to the cognitive and medical sequelae of the disorder.

• Apathy: Apathy and lack of motivation are common, which can be mistaken for depression.

• Emotional Lability: Individuals may experience rapid changes in mood, with episodes of crying or laughing that are disproportionate or inappropriate to the context.

Behavioral Symptoms

• Impulsivity and Poor Judgment: Some individuals may show impulsivity and poor judgment, linked to executive dysfunction.

• Social Inappropriateness: There may be instances of socially inappropriate behavior, again possibly related to impaired executive functions.

Physical and Motor Symptoms

• In addition to cognitive symptoms, physical and motor symptoms such as weakness, tremors, or difficulty walking can be present, reflecting the brain areas affected by strokes or other vascular injuries.

Treatment Plans

The detection of statistically and clinically meaningful change over time is always a critical component of neuropsychology practice. Of course, variation is inherent in re-evaluation of any healthcare measure and the interpretation of change can be important in our understanding of progression or recovery. Interpretations of neuro- psychological changes require careful consideration of large databases for normative performances to make determinations of statistical significance or clinical meaning. Unlike the gradual progression typical of Alzheimer’s disease, VCID often shows a stepwise decline, with periods of rapid worsening following strokes or other vascular events, interspersed with periods of stability. Many existing diagnostic schemes for VCID cite a “clear temporal relationship” between a cerebrovascular event and the acute onset of cognitive symptoms. This is often more observable when the underlying pathology involves a single large stroke or strategic infarct, but it is more challenging to capture in the cases where the primary pathology is small vessel disease or leukoaraiosis. In practice, VCID often involves a mix of several vascular pathologies and/or mixed dementia. As a result, these expectations about its onset and progression tend to more often be the exception rather than the rule. Because the progression of VCID can vary markedly across individuals, it can be challenging to determine prognostic outcomes. To this end, serial neuropsychological evaluations can generate helpful metrics to quantify the degree and directionality of cognitive changes over time, which can be useful in determining differential diagnoses and treatment effects. Using reliable change indices when available, neuropsychologists can derive quantitative estimates of change in patients’ performances that statistically account for random measurement error and/or practice effects. This can yield more precise and sensitive indicators of change that are both statistically and clinically meaningful.

Given its heterogeneity, care for vascular impairment and dementia must be personalized, taking into account the individual’s overall health, comorbid conditions, and risk factors. Comprehensive neuropsychological evaluation can help clarify the treatment plan in many instances. Regular monitoring and adjustments to the treatment plan are necessary to address the progression of the disease and emerging health issues. Non-pharmacological interventions, such as lifestyle modifications, physical activity, and cognitive therapies, also play a crucial role in the management of VCID and should be integrated into the care plan alongside medication therapy.

Lifestyle modification is especially important to mitigate further vascular risk, including smoking cessation, dietary modification, and limiting alcohol use. There have also been several clinical trials investigating the effects of exercise on outcomes in individuals with VCID^23–25. Exercise is recognized for its potential benefits on cognitive function, physical health, and overall well-being, making it a promising non-pharmacological intervention for dementia, including VCID. These studies vary in their design, the type of exercise interventions tested, and the outcomes measured, but generally, they explore how regular physical activity might improve cognitive functions, physical capabilities, quality of life, and daily living activities in people with VCID. Some key findings are summarized in Box 3.

Box 3: Findings from Clinical Trials on Exercise in VCID:

1. Improved Cognitive function: Some trials have reported that aerobic exercise, strength training, or a combination of both can lead to improvements in cognitive performance, particularly in executive functions and attention.

2. Enhanced Physical Health: Exercise interventions have been shown to improve physical health outcomes, such as increased endurance, strength, balance, and mobility. These improvements can help reduce the risk of falls and improve the overall ability to perform daily activities.

3. Better Quality of Life: Regular physical activity may also contribute to improvements in mood, reduction in symptoms of depression, and overall enhancements in the quality of life for individuals with VCID and their caregivers.

4. Neuroplasticity and Brain Health: While more research is needed, research has suggested that exercise can promote neuroplasticity, potentially improving brain health and function through mechanisms such as increased cerebral blood flow and the stimulation of neurotrophic factors.

The neuropsychological evaluation can be particularly informative in developing strategies for targeted cognitive rehabilitation treatments or strategies following a cerebrovascular event. A comprehensive neuropsychological evaluation typically assesses not only cognitive function, but also considers other psychological factors, physical health (e.g., pain, fatigue, sleep problems, hearing difficulties) and environmental supports that can influence cognitive recovery. In this way, neuropsychology can provide a thorough understanding of a patient’s deficits along with their preserved areas of functioning, which is critical to the selection of rehabilitation techniques that can be exercised to promote functional gains in daily life. To this end, several systematic reviews of cognitive rehabilitation strategies for VCID have provided evidence-based guidelines for interventions addressing cognitive deficits. For example, Cicerone and colleagues (2019) provide practice standards for cognitive impairments related to deficits in attention, visual scanning issues (i.e., for neglect after right-hemisphere stroke), mild memory deficits, language deficits after left-hemisphere stroke, social-communication problems, metacognitive strategy training for deficits in executive functioning; and comprehensive-holistic neuropsychological rehabilitation to reduce cognitive and functional disability²⁶. Box 4 provides a case example demonstrating how neuropsychological findings can be used to generate relevant compensatory strategies that can facilitate functioning in daily life. In this case, the neuropsychologist reviewed the findings with the patient and her caregiver, and they collaboratively discussed how these strategies could be applied in various aspects of the patient’s daily life to improve communication and enhance functional independence.

Box 4: Case Example of Neuropsychologically-Informed Compensatory Strategies.

Ms. Smith is a 67-year-old female with history of left parietotemporal ischemic stroke and diffuse chronic microvascular disease observed on neuroimaging. Neuropsychological findings were used to generate tailored compensatory strategies, such as

1. Organizational and working memory deficits: As she was prone to becoming cognitively overwhelmed, she can divide complex tasks into small, manageable units. Write out clearly the steps involved in each component and use a checklist to ensure no steps are missed.

2. Verbal learning difficulties: She benefitted notably from repetition, so she should request repetition of important information when possible (e.g., from medical providers, when scheduling activities with friends).

3. Verbal retrieval deficits: Visual memory was strong, so she can integrate visual aids, like charts, calendars and graphs, to track daily activities and schedules. As her verbal recall benefitted from cuing, she can use notes to jog her memory of important events or conversations.

4. Attentional deficits: She can proactively minimize distractions in her environment (e.g., turn off phone, TV) when having conversations with others and ask for information to be repeated if she becomes distracted.

5. Slowed processing speed: Ensure additional time is allotted in her daily schedule for the completion of important tasks. Ask others to present important information at reduced pace and summarize or repeat back information to ensure understanding.

In addition to patient-focused interventions, neuropsychological findings can also provide useful recommendations regarding caregiver support needs, psychoeducation, and direct training of the patient with the caregiver. Such interventions can render benefits for both the caregiver and patient alike. A review of caregiver interventions found that interventions transferred beneficially to patients by reducing neuropsychiatric symptoms as well as behavioral and mood disturbances, enhancing cognition and quality of life, and delaying institutionalization and mortality²⁷. Perhaps more notably, neuropsychology services can provide relevant information for patients and their caregivers regarding level of care needed at present and in the future, so as to more effectively plan for issues such as eventual loss of capacity, driving safety, necessary environmental modifications for safety in the home, referral to appropriate community resources for respite care and/or in home supportive services, and long-term planning for residential care option (e.g., assisted living or skilled nursing facility).

Management of genetic vasculopathies is a somewhat unique application within the spectrum of VCID disorders that often involves multidisciplinary care, including genetic counseling, surveillance for vascular complications, and interventions to prevent or treat vascular events (e.g., surgical repair of aneurysms). Because of the inherited nature of these conditions, genetic counseling and testing of family members is typically recommended. Understanding the specific genetic and molecular pathways involved in these conditions has implications for targeted therapies and personalized medicine approaches in the future.

Summary

VCID encompasses a heterogenous and complex spectrum of disorders that accounts for a sizeable proportion of cognitive impairment in older adults. With advancements in acute stroke care and an ageing population with high incidence of obesity and diabetes-related conditions, it may be expected that increasingly more patients with history of stroke and/or cerebrovascular disease will require ongoing management and evaluation of vascular-related cognitive difficulties. Neuropsychology can assist with differential diagnosis, early detection and ongoing monitoring of cognitive impairments in VCID. Integration of neuropsychology findings into treatment planning can also provide useful tools for patients and caregivers to maximize functional capacity and improve quality of life throughout the disease course.

Key points:

• Neuropsychological assessment can provide added value to the assessment and treatment planning for persons with vascular contributions to cognitive impairment and dementia.

• Systematic reviews and meta-analyses have suggested that neuropsychological assessments can provide differential diagnostic value between persons with primary Alzheimer’s disease and those with primary Vascular Dementia.

• Neuropsychological assessment can provide information to patients and families to help them use compensatory techniques for weaknesses and maximize functional capacity and quality of life throughout the course of disease.

Clinical Care Points:

• Neuropsychology assists with differential diagnosis and prediction of cognitive course in vascular cognitive decline.

• Comprehensive neuropsychological assessment allows for more individualized treatment planning than a brief cognitive screening.

• Pathophysiology, size, and location of lesions are not directly associated with cognitive, behavioral, nor functional outcomes so neuropsychological assessment can clarify patient-reported outcomes and objectively measured impairments.