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Section 7.2

Vascular cognitive impairment and dementia

4th Edition
2012-2013 UPDATE
March 19, 2013

2012 Definition of Vascular Cognitive Impairment:

Vascular Cognitive Impairment (VCI) includes the cognitive and behavioural disorders associated with cerebrovascular disease and risk factors, from mild cognitive deficits to frank dementia.  VCI is a syndrome with cognitive impairment affecting at least one cognitive domain (e.g., attention, memory, language, perception or executive function) and with evidence of clinical stroke or subclinical vascular brain injury.  VCI encompasses a large range of cognitive deficits, from relatively mild cognitive impairment of vascular origin (VaMCI) to Vascular Dementia (VaD), the most severe form of VCI.  VCI also plays an important role in patients with Alzheimer’s disease (AD) pathology who have coexisting vascular lesions.

Cognitive deficits:  The pattern of cognitive deficits in VCI may encompass all cognitive domains, including focal stroke syndromes, but there is likely to be an underlay or preponderance of attention and executive function deficits, such as slowed information processing, impairments in the ability to maintain task set or shift from one task to another and deficits in the ability to hold and manipulate information (e.g., working memory).

Vascular pathology:  Cognitive impairment can result from a range of vascular pathology, including multiple cortical infarcts, multiple subcortical infarcts, covert (“silent”) infarcts, strategic infarcts, small-vessel disease with white matter lesions and lacunae, and brain hemorrhage.

Diagnosis criteria for vascular cognitive impairment following stroke has been defined by Gorelick et al (2011) and can be found in Table 7.2A. 

All patients with vascular risk factors and those with clinically evident stroke or transient ischemic attack should be considered at increased risk for vascular cognitive impairment (VCI), particularly those patients with cognitive, perceptual or functional changes that are clinically evident or reported during history taking.

7.2.1   Screening and Assessment

  1. Patients with significant vascular risk factors for VCI, such as hypertension, diabetes, transient ischemic attack or clinical stroke, neuroimaging findings of covert stroke or white matter disease, hypertension-associated damage to other target organs, atrial fibrillation, other cardiac disease, and/or sleep apnea should be considered for VCI screening. [Evidence Level A]
  2. Screening for VCI should be conducted using a validated screening tool, such as the Montreal Cognitive Assessment test [Evidence Level C]. Refer to Table 7.2B under Implementation Resources for information about selected tools and their psychometric properties. (Table 7.2B)
  3. Screening to investigate a person’s cognitive status should address arousal, alertness, attention, orientation, memory, language, agnosia, visual-spatial/perceptual function, praxis, and executive function.  Executive function screening may include assessment of initiation, insight, planning and organization, judgment, problem solving, abstract reasoning, and social cognition [Evidence Level C].
  4. Post-stroke patients with suspected cognitive impairment should also be screened for depression, given that depression has been found to contribute to vascular cognitive impairment. A validated screening tool for depression should be used [Evidence Level A]. Refer to recommendation 7.1 for additional information
  5. Patients who demonstrate cognitive impairments in the screening process should be managed by a healthcare professional with expertise in the assessment and management of neurocognitive functioning.* This assessment should include cognition, perception and/or function as appropriate to guide comprehensive management [Evidence Level B].  If required, a referral should be made to an appropriate cognitive specialist [Evidence Level C].
    1.  Additional assessments should be undertaken to determine: the nature and severity of cognitive impairments; the presence of remaining cognitive abilities and straights;
    2. The impact of deficits on function and safety in activities of daily living and instrumental activities of daily living, and occupational and school functioning should also be assessed.
    3. The results of these assessments should be used to guide selection and implementation of appropriate remedial, compensatory and/or adaptive intervention strategies according to client-centred goals and current or anticipated living environment (e.g., to help with discharge planning). [Evidence Level B].

* Experts in neurocognitive assessment may include a neuropsychologist, psychologist, occupational therapist, speech-language pathologist, clinical nurse specialist, psychiatrist, physiatrist, geriatrician, neurologist, and developmental pediatricians.  Experts require specific qualifications to administer many of the identified assessments.

7.2.2   Timing of Screening and Assessments

  1. All patients considered at high risk for cognitive impairment should be assessed periodically throughout the stages of care as indicated by the severity of clinical presentation, history and/or imaging abnormalities to identify cognitive, perceptual deficits, depression, delirium and/or changes in function [Evidence Level C].
  2.  Stages of care across the continuum may include:
    1. during presentation to emergency when cognitive, perceptual or functional concerns are noted;
    2. during acute care stay, particularly if cognitive, perceptual or functional concerns, or evidence of delirium is noted;
    3. throughout rehabilitation within inpatient, outpatient, and home-based settings, according to client progress;
    4. following hospital discharge from the emergency department or inpatient setting to an outpatient or community-based healthcare setting.
  3. While assessment at different stages of care is important for guiding diagnosis and management, it is also important to be aware of the potential impact of multiple assessments on both the validity of the results as well as on the patient (e.g., test fatigue, practice effects).  [Evidence Level B].
  4. Effects of age must also be considered, particularly in children with stroke where outcomes will evolve in parallel with development and deficits may not be fully realized until many years later [Evidence Level C]

7.2.3   Management of Vascular Cognitive Impairment

  1. Vascular risk factors (e.g., hypertension, atrial fibrillation) should be managed aggressively to achieve optimal control of the pathology underlying cognitive impairment following a stroke or TIA [Evidence Level A]. Refer to section 2, Prevention of Stroke,  for additional information
  2. Interventions should be tailored according to the following considerations:
    1. Goals should be patient-centred and sensitive to the values and expectations of patient, family and caregivers  [Evidence Level B]
    2. Goals should be developed in the context of both the cognitive impairments as well as patients’ intact cognitive abilities, with the aim to facilitate resumption of desired activities and participation (e.g., self-care, home management, leisure, social roles, driving, volunteer participation, financial management, return to work) [Evidence Level B]
      NOTE: Issues such as intensity and dose of therapy, stage of treatment, and impact of severity of deficits can modify effectiveness of therapy, and require more research.
  3. Evidence for interventions for cognitive impairment is growing, although more research is required.  Interventions with the patient can be broadly classified as either compensatory strategy training, or direct remediation/cognitive skill training.  These approaches are not mutually exclusive, and, depending upon the impairments and goals, may be offered together.
    NOTE:  It should be noted, however that if the level of impairment has reached the moderate dementia stage, interventions may be more focused on providing education and support for the caregiver in addition to, or in lieu of, cognitive rehabilitation with the patient. 

    1. Compensatory Strategy training focuses on teaching strategies to address impairments and is often directed at specific functional limitations in activities of daily living to promote independence. Compensatory strategies can include learning to use external devices (e.g., memory notebooks or alarms), adapting the external environment (e.g., additional social supports or reorganization of living space), and/or learning to use internal mental operations or processes (e.g., problem-solving techniques) that enhance the impaired cognitive domain.  Certain types of strategy training have been shown to be effective for improving attention, memory, language, praxis and executive function domains. [Evidence Level B].
    2. Direct remediation/cognitive skill training focuses on providing intensive specific training to directly improve the impaired cognitive domain. Computer-based training has been shown to be effective in improving attention and working memory impairments as well as language impairments [Evidence Level B]. The impact of direct skill training on achievement of goals at the activities and participation levels of functioning requires more research.
    3. New developments in cognitive intervention that may be of potential benefit include repetitive transcranial magnetic stimulation or direct stimulation, the use of virtual reality environments or simulations, and application of constraint-induced therapy for the impaired cognitive domain.  These strategies require more research before recommendations can be developed on their use.
  4. Patients with cognitive impairment and evidence of changes in mood (e.g., depression, anxiety), or behavioural changes on screening should be referred and managed by an appropriate mental healthcare professional [Evidence Level B].  Refer to recommendation 7.1 for additional information.

7.2.4   Pharmacotherapy for Vascular Cognitive Impairment

  1. Patients with evidence of vascular cognitive impairment should be managed by a physician with expertise in vascular cognitive impairment for further assessment and recommendations regarding pharmacotherapy [Evidence Level C].
  2. Cholinesterase inhibitors should be considered for management of vascular cognitive impairment diagnosed using the National Institute of Neurological Disorders and Stroke (NINDS) – Association Internationale pour la Recherche et l’Enseignement en Neurosciences (AIREN) diagnostic criteria [Evidence Level B].
    1. There is fair evidence of small magnitude benefits for donepezil in cognitive and functional outcomes, with less robust benefits on global measures [Evidence Level B]. Donepezil can be considered as a treatment option for vascular dementia. More research is needed on the benefits of donepezil for vascular cognitive impairment.
    2. There is fair evidence of small magnitude benefits for galantamine on cognition function and behaviour in mixed Alzheimer and cerebrovascular disease. Galantamine can be considered a treatment option for mixed Alzheimer and cerebrovascular disease [Evidence Level B].
    Rationale

    Vascular cognitive impairment affects up to 60 percent of stroke survivors and is associated with poorer recovery and decreased function in activities of daily living and instrumental activities of daily living. Patients may require long-term, ongoing intervention and rehabilitation (Teasel et al, 2009;  Madureira et al 2001). Cognitive abilities in the areas of executive function, attention and memory appear important in predicting functional status at discharge.  In addition, cognitive impairment can be chronic and progressive after stroke; post-stroke dementia is estimated to occur in 26 percent of stroke patients by three months (95% CI 3% in age-matched controls) and adversely affects recovery. Cognitive impairment increases long-term dependence and is associated with increased mortality rates (61 percent versus 25 percent) (Black, 2007).

    Cognitive impairment due to covert vascular pathology is also increasing. Covert strokes, usually lacunes, are common (23 percent of community elderly) and are associated with cognitive decline, dementia, and stroke. Evidence is emerging that demonstrates that for every clinically evident stroke, there may be up to ten “covert” strokes. Signs of covert stroke are often manifested as signs and symptoms of cognitive impairment. Intracerebral small-vessel disease is a disorder that is on the rise with the aging of the population, leading to an increase in the need for long-term care support services.

    Emotional and related behavioural changes are known to occur following stroke, with specific behaviours linked to the affected hemisphere and stroke location.  Disorders such as apathy, anxiety, labile laughing and crying, and other behaviours such as disinhibition, denial, indifference, overt sadness, and aggressiveness can occur in the early days following stroke. Some of these behaviours may be related to later development of depression, however, prospective studies of mood changes during and immediately after stroke are limited as yet.

    In most population studies, vascular dementia is the second most common cause of dementia, after Alzheimer disease.  The combination of Alzheimer disease and vascular disease results in the commonest substrate of dementia in the elderly. A single macroscopic hemispheric infarct is sufficient to cause dementia in people with intermediate Alzheimer pathology.

    System Implications

    •        Public education to increase awareness that cognitive changes may be considered as manifestations of vascular disease and stroke.

    •        Public education to increase awareness of untreated or uncontrolled hypertension and other vascular risk factors and their relationship to cognitive changes and dementia.

    •        Professional education to increase awareness among family physicians that patients with vascular risk factors, if not treated, will be at high risk for cognitive deficits.

    •        Professional education across specialties (e.g., nephrology, ophthalmology, family medicine) to increase awareness that patients with small-vessel disease should be investigated for stroke risk factors and cognitive impairment.

    •        Access to interprofessional teams with the expertise to appropriately manage patients with vascular cognitive impairment across the continuum of stroke care and in the community.

    •        Continuing professional education to ensure proficiency in assessment administration, interpretation and management of patients demonstrating post stroke and vascular cognitive impairment or at risk of vascular cognitive impairment.

    Performance Measures

    1. Percentage of patients with stroke or stroke risk factors who undergo a brief cognitive screening at each transition point along the continuum of stroke care (i.e., acute inpatient care, inpatient rehabilitation, outpatient clinics and programs, home-based services, and stroke prevention clinics) and in the community following inpatient discharge and at any time when there is a suspected change in cognitive status. (Core indicator)
    2. Percentage of patients with stroke who are referred for more in-depth cognitive or neuropsychological assessment throughout the continuum of stroke care (for example, during inpatient care, inpatient rehabilitation, outpatient and ambulatory clinics or programs (stroke prevention clinics) and/or following inpatient discharge to the community).
    3. Percentage of change in Montreal Cognitive Assessment (MoCA) scores at baseline and three months, six months and one year following initiation of therapy.
    4. Percentage improvement in control of high blood pressure and other vascular risk factors in patients with vascular cognitive impairment.

    Measurement Notes

    • 7.2 and corresponding performance measures apply across the continuum of stroke care and should be considered in acute inpatient care, inpatient rehabilitation, outpatient clinics, home-based services, and stroke prevention clinics and/or following inpatient discharge to the community.
    • When using these performance measures it is important to record when and in what context (continuum of care) the measurements were conducted. Data for measurement may be found through primary chart audit. Data quality will be dependent on the quality of documentation by healthcare professionals.
    • This is a new area and will require a great deal of education for healthcare professionals especially in the area of documentation.
     
    Implementation Resources and Knowledge Transfer Tools
    Summary of the Evidence

    It has been estimated that 5% of all people over the age of 65 years, in Canada, have evidence of vascular cognitive impairment (Rockwood et al. 2000). However, in individuals who have experienced stroke, reported prevalence rates tend to be much greater, ranging from 15 – 20% in various clinical settings to 39%, 35%, 30% and 32% at 3 months, one year, 2 years and 3 years post stroke, respectively, as reported by Patel et al. (2003). While the risk for cognitive impairment is greater following stroke and, certainly, not all individuals with cognitive impairment have dementia, post-stroke cognitive impairment is associated with an increased risk for dementia.
    Pendlebury and Rothwell (2009) conducted a systematic review and meta-analysis of 73 published studies examining prevalence and predictors of dementia in individuals with stroke. Overall, pooled prevalence of pre-stroke dementia was 14.4% in hospital-based cohorts (n=22) and 9.1% in community-based studies (n=8). Prevalence of post-stroke dementia ranged from 7.4% in population-based studies of individuals with first-ever stroke and no existing dementia to 41.3% in hospital-based studies of individuals with recurrent stroke (both with and without existing dementia). Rates of dementia were at least doubled following recurrent stroke when compared to first-ever stroke and were higher in hospital-based than in community-based studies. At 3- 6 months, post-stroke incidence of dementia was approximately 20%; this increased linearly at a rate of 3.0% in hospital-based studies of either first or recurrent stroke. Incidence rates were lower in population-based studies of first-ever stroke and when cases with recurrent stroke were excluded.

    In the review by Pendlebury and Rothwell (2009), multivariate analyses were identified in 19 studies. From these 19 studies, the most commonly reported independent predictors of post-stroke dementia were older age, lower education level, previous stroke, diabetes, atrial fibrillation, existing cognitive impairment and stroke severity. In summary, Pendlebury and Rothwell (2009) suggest that approximately 10% of patients have existing dementia at the time of stroke. An additional 10% develop new dementia shortly after a first-ever stroke while more than one-third of patients may experience dementia following a recurrent stroke. Recurrent stroke was identified as an important, and commonly cited, predictor of dementia. Gorelick (1997, 2004) reported on the risk factors for vascular dementia in 4 categories: demographic (older age, male sex, lower level of education), atherosclerotic (hypertension, smoking, myocardial infarction, diabetes, hyperlipidemia), genetic (cerebral autosomal dominant arteriopathy with subcortical infarct, leukoencephalopathy, apolipoprotein) and stroke-related (volume of cerebral tissue loss, evidence of bilateral cerebral infarction, strategic infarction, white matter disease).
    Cognitive impairment following stroke has been associated with reduction in functional ability, and increased risk for depression (ebrsr.com). Individuals with cognitive impairments may require more therapy over longer periods of time (Zinn et al. 2004). In addition, the presence of executive dysfunction may have a negative impact on engagement in rehabilitation (Skidmore et al. 2010). A review by Leys et al. (2005) reported that higher rates of mortality have also been found among patients with post stroke dementia in both community-based and hospital-based studies. Overall, mortality rates are reported to be 2 to 6 times higher among individuals with post stroke dementia after adjusting for demographic factors, associated cardiac disease, stroke severity and stroke recurrence (Leys et al. 2005).

    At present, there is no ‘gold standard’ for the diagnosis of vascular dementia. However, it has been recommended that given the anticipated presence of executive dysfunction in cases of vascular cognitive impairment post stroke, any assessment used to detect the presence of VCI be appropriate to the assessment of executive function. As part of the development of the Canadian Stroke Network vascular cognitive impairment harmonization standards, Hachinski et al. (2006) recommended use of a 5-minute neuropsychological protocol for the identification of VCI that included selected subtests of the Montreal Cognitive Assessment (5-word memory task – registration, recall, recognition, 6-item orientation and 1-letter phonemic fluency). This could be supplemented with a cube and clock drawing task, a short Trails B test and other brief attention language and abstraction tasks. Given more time, the original Trails-making test, a semantic fluency test or the MMSE could be added (if administered on a different day or more than one hour following the 5-minute protocol). Inclusion of the Mini Mental Status Examination in the initial 5-minute protocol was rejected, as it does not provide adequate assessment of executive function and is insensitive to mild memory impairment (Hachinski et al. 2006).

    Evidence for cognitive rehabilitation interventions within the stroke population is not strong in many areas. In general, interventions may be considered to have one of two objectives: 1) to reinforce or re-establish previous behavioural skills or function (to remediate) or 2) to establish new patterns of activity or behaviour through compensatory mechanisms that may be either internal or external to the individual (Cicerone 2000, 2005). A meta-analytic examination of the 2 systematic reviews of cognitive rehabilitation interventions conducted by Cicerone et al. (2000, 2005, ) and updated in 2011, reported effect sizes for cognitive interventions in attention, visuospatial, language, memory and comprehensive training. Overall, cognitive rehabilitation interventions were associated with small, but significant treatment effects (ES=0.30). Overall treatment effect was moderated by treatment domain, etiology of injury (e.g. TBI vs. stroke) and time since injury. For studies of individuals with stroke, the reported pooled effect size associated with cognitive rehabilitation was slightly larger (ES=0.40) than the overall effect size; however, it should be noted that these were primarily in the areas of language and visuospatial deficits (Cicerone et al. 2005). Studies of attention or executive function, memory or comprehensive cognitive function were focused more often on individuals with TBI or other brain injury. Although generally positive results have been reported for studies examining the use of attention training, memory strategy training, use of mnemonic devices (e.g. personal pagers), and problem-solving training for study participants who have experienced brain injury (including stroke) evidence from randomized controlled trials specific to the stroke population is limited (Cicerone et al, 2011; ebrsr.com).

    Pharmacotherapy
    Cholinergic agents have been used in the treatment of dementia of the Alzheimer’s type. Three such agents, donepezil, rivastigmine and galantamine, have also been investigated for use in the treatment of vascular dementia. Donepezil, a selective acetylcholinesterase inhibitor, has been the subject of 3 large randomized controlled trials (Black et al. 2003, Wilkinson et al. 2003, Roman et al. 2010). A meta-analysis of the first 2 trials demonstrated significant improvements in cognitive and global function, including improvements in the performance of activities of daily living associated with use of donepezil in the treatment of patients with mild to moderate vascular dementia (Passmore et al. 2005). The most recent trial also reported significant improvement in cognitive outcomes associated with treatment (Roman et al. 2010).
    Galantamine is an acetylcholinesterase inhibitor that has been shown to be of benefit in terms of cognition, behaviour and the performance of activities of daily living when used in the treatment of Alzheimer’s dementia (Erkinjuntti et al. 2002, 2003); however the benefit associated with treatment was most obvious in a subgroup of individuals with mixed dementia (Alzheimer’s Disease plus cerebrovascular disease) (Erkinjuntti et al. 2002).

    Children and Vascular Cognitive Impairment
    Cognitive outcomes for children with stroke must be considered differently. Covert VCI is not a common issue except in select disease states (moyamoya, sickle-cell, small vessel vasculitis). Most importantly, cognitive outcomes must be considered within the context of constantly evolving neurodevelopment. Thus, outcomes must use developmentally and age-appropriate outcome measures. Deficits in cognition and higher brain functions may not be evident until the relevant stage of development is reached, whereby young children “grow into” their deficits over time.[Westmacott et al. 2007a;Westmacott et al. 2009]

    About 1 in 3 children with stroke have cognitive deficits at outcome, limiting academic, social, and independent functional success [Friefeld et al. 2004;Nass and Trauner 2004](Carr L 2011). Adverse cognitive outcomes from childhood cerebral sinus venous thrombosis (CSVT) [Wasay et al. 2008;deVeber et al. 2001;Moharir et al. 2010;Berfelo et al. 2010] and hemorrhagic stroke [Blom et al. 2003;Meyer-Heim and Boltshauser 2003] are also common. Overall cognitive function including intelligence, verbal ability, working memory, and processing speed are lower than average in children with stroke. (Westmacott, 2009), [Hetherington et al. 2005; McLinden et al. 2007] [Max 2004; Lansing et al. 2004].

    Post-stroke psychiatric/behavioural disorders also appear to be common in childhood stroke (Max, 2002; Elbers 2013). Difficulties with social and behavioral development are also increased in children after stroke with secondary impact on parental mental health (De Schryver, 2002; Goodman, 2000). Limited studies suggest that social function is commonly impaired following stroke in childhood [Mosch et al. 2005]. Rates of potentially treatable Attention Deficit Hyperactivity Disorder (ADHD) are increased [Max et al. 2002;Max et al. 2003;Max et al. 2004], particularly with lesions involving the putamen [Teicher et al. 2000].

    Contradicting the idea that the immature brain may be more plastic with a greater capacity for recovery, a younger age at stroke may be associated with worse cognitive and behavioural outcomes. (Westmacott, 2009; Everts, 2008)[Stiles 2000;Lansing, Max, Delis, Fox, Lancaster, Manes, and Schatz2004;Westmacott et al. 2007b]. There is also evidence for late emergence of cognitive deficits after perinatal stroke, with IQ measured in the preschool period higher than that measured later.(Westmacott, 2011) About one third of childhood stroke survivors require specialized education (Delsing, 2001). Regular, age-appropriate neuropsychological evaluations should be considered in all at-risk children to determine educational and support needs.

    Evidence Tables:

    1. Vascular Cognitive Impairment and Dementia: Screening and Assessment
    2. Vascular Cognitive Impairment and Dementia: Management Review