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Mood, Cognition and Fatigue following Stroke

2. Vascular Cognitive Impairment

Sixth Edition, 2019 UPDATE

Definitions and Descriptions

Vascular Cognitive Impairment: Includes the cognitive and behavioural disorders associated with cerebrovascular disease and risk factors, from mild cognitive deficits to frank dementia.  Vascular cognitive impairment 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.  Vascular cognitive impairment encompasses a large range of cognitive deficits, from relatively mild cognitive impairment of vascular origin to vascular dementia, the most severe form of vascular cognitive impairment.  Vascular cognitive impairment also plays an important role in people with Alzheimer’s disease pathology who have coexisting vascular lesions.  Diagnostic criteria for vascular cognitive impairment following stroke has been defined by Gorelick et al (2011), with further revisions by the VASCOG society (2014) and can be found in Table 2A  

Cognitive deficits: The pattern of cognitive deficits in vascular cognitive impairment may encompass any cognitive domain (see Sachdev et al., 2014, Table 1). The most common areas are attention, processing speed, and frontal-executive function (which includes functions such as planning, decision making, judgment, error correction, impairments in the ability to maintain task set, inhibit a response, or shift from one task to another) and deficits in the ability to hold and manipulate information (e.g., working memory). Other cognitive domains that could be affected include learning and memory (immediate, recent and recognition memory), language (expressive, receptive, naming, grammar and syntax), visuoconstructional-perceptual ability, praxis-gnosis-body schema, and social cognition. 

Vascular pathology: Cognitive impairment can result from a range of vascular pathologies (see Sachdev et al., 2014, Table 3), including large or multiple cortical infarcts, multiple subcortical infarcts, covert (“silent”) infarcts, strategic infarcts, small-vessel disease (ischemic white matter changes, multiple lacunar infarcts, dilatation of perivascular spaces, cortical microinfarcts and microhemorrhages), and brain hemorrhage.  Risk factors such as hypertension, diabetes and focal or global cerebral hypoperfusion are also associated with cognitive impairment. 

2.0 Vascular Cognitive Impairment

All people with clinically evident stroke or transient ischemic attack should be considered at risk for vascular cognitive impairment [Evidence Level B].

Note: Screening and assessment of vascular cognitive impairment must be nuanced by multiple factors. In the current version of these recommendations we have included a section called “clinical considerations”, where we present a brief discussion of issues identified in the evidence review or by expert consensus that impact performance or interpretation of cognitive screening and assessment information – please see below.

2.1 Screening for Vascular Cognitive Impairment
  1. People who have experienced a stroke or transient ischemic attack should be considered for screening for vascular cognitive impairment [Evidence Level C]. This may occur prior to discharge from acute care if concerns with cognition are identified; during inpatient rehabilitation, and during post-stroke follow up in outpatient and community settings [Evidence Level C].
  2. People who have experienced a stroke with other significant risk factors for vascular disease and vascular cognitive impairment, such as neuroimaging findings of covert stroke or white matter disease, hypertension, diabetes, atrial fibrillation, or other cardiac disease may be considered for screening for vascular cognitive impairment, particularly those people who have experienced a stroke with cognitive, perceptual or functional changes that are clinically evident or reported during history taking [Evidence Level B].
  3. Screening for vascular cognitive impairment should be conducted using a validated screening tool, such as the Montreal Cognitive Assessment screen [Evidence Level B]. Refer to Table 2B for a summary of suggested vascular cognitive impairment screening and assessment tools, and psychometric properties.

Note: Screening of global cognitive functioning using a validated tool can be administered to objectively understand the functional impact of vascular cognitive impairment.

Stages of care across the continuum may include:  

  • During acute care stay, particularly if cognitive, perceptual or functional concerns, in the absence of delirium is noted; 
  • During rehabilitation in inpatient, outpatient, and home-based settings, according to client progress; 
  • Following hospital discharge from the emergency department or inpatient setting to follow-up in an outpatient or community-based healthcare setting.
2.2 Assessment for Vascular Cognitive Impairment
  1. The diagnosis of vascular cognitive impairment requires confirmation of cerebrovascular disease.  Brain imaging with computed tomography (CT) or magnetic resonance imaging (MRI) is useful to evaluate cerebrovascular disease [Evidence Level B].  
    1. MRI is more sensitive than CT to vascular changes.
    2. Clinical history and examination findings consistent with stroke can be used as objective evidence of cerebrovascular disease if imaging is not available.
  2. People who have experienced a stroke and who demonstrate cognitive impairments (either clinically, by history, by report of the individual or family, or detected in the screening process) should be assessed by healthcare professionals with the appropriate expertise in neurocognitive functioning, ideally by a clinical neuropsychologist [Evidence Level C].  
  3. The impact of deficits on function and safety in activities of daily living, instrumental activities of daily living, occupational function and/or academic functioning should be considered as part of a cognitive assessment (e.g., driving, home safety) [Evidence Level C]. 
  4. People who have experienced a stroke with suspected cognitive impairment should also be screened for depression, given that depression has been found to contribute to vascular cognitive impairment [Evidence Level B] Refer to Recommendation 1.0 on Post-stroke Depression for additional information.
  5. Prior to discharge or transfer from acute care or inpatient rehabilitation, people with acute cognitive problems following stroke should receive an assessment for any safety risks from persisting cognitive impairments and this should be communicated to their primary care team [Evidence Level C].
  6. The results of these assessments should be considered to guide selection and implementation of appropriate remedial, compensatory and/or adaptive intervention strategies according to person-centered needs and goals [Evidence Level C].
  7. People who have experienced a stroke should have a full assessment of their cognitive strengths and weaknesses when undergoing rehabilitation or prior to returning to cognitively demanding activities such as driving or work [Evidence Level C].

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

Clinical Considerations for Screening and Assessment of Vascular Cognitive Impairment (Statements moved from recommendations sections for 2019)

  1. Vascular cognitive impairment can be associated with a range of deficits. Further assessment could be considered to evaluate impairments in arousal, alertness, sensorimotor function, attention, orientation, memory, language, agnosia, visual-spatial/perceptual function, praxis, information processing speed, and executive function.  
    1. Attention, speed of processing and executive function domains are commonly affected post stroke. Executive function abilities to be assessed may include initiation, inhibition, shifting, insight, planning and organization, judgment, problem solving, abstract reasoning, and social cognition.
  2. Assessment Tool Selection: Cognitive evaluation may be conducted using standardized assessments to determine the nature and severity of cognitive impairments, as well as the presence of remaining cognitive abilities and strengths.
    1. Therapeutic activities and/or functional observations may provide additional information by showing the impact of impairments. 
    2. The tools used to assess vascular cognitive impairment may be unique to different settings, geographical areas, professions and timelines encountered along the continuum of care.  Consider the validity and standardization of the selected tools with regards to factors such as age, sex, language, aphasia and education levels.
  3. Comorbidities: Screening or assessment for vascular cognitive impairment should take into account any immediate factors that may impact interpretation of results, such as communication and sensorimotor deficits (speech and language, vision, hearing), delirium, hypo-arousal, neuropsychiatric symptoms (e.g., depression, apathy and anxiety) and other medical conditions that may have a temporary impact on cognition.
  4. Timing: The impact and presentation of vascular cognitive impairment can evolve over time.  Screening and assessment of people who have experienced a stroke and considered at risk for cognitive impairment should be undertaken at different stages of care (rehabilitation, transition points, community follow-up) as indicated by the severity of clinical presentation, comorbidities, history and/or imaging abnormalities and needs or goals of the person with stroke and their caregiver.
  5. Multiple Assessments: Although screening or conducting assessments 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 person following stroke (e.g., practice effects, test fatigue).  To avoid practice effects, the use of different equivalent assessment forms is recommended when available (e.g., MoCA has three versions).
  6. Life Stage: Effects of age, developmental stage or pre-stroke function should be considered when deciding when and what to assess.  Decisions about what to assess should always take into consideration person-centered goals which may differ by life stages.
  7. Capacity: Professionals should consider the capacity of the person with stroke for making informed choices and decisions.  Capacity related provincial legislation should be reviewed, and appropriate substitute decision makers should be identified if the person is deemed incapable of making specific decisions regarding their personal health care, or self-management following discharge. In special circumstances, when abilities are in question, an individual can be referred to a third party, designated Capacity Assessor to determine a person's mental capacity to make decisions about property, finances and personal care.
2.3 Management of Vascular Cognitive Impairment following Stroke
  1. Vascular risk factors (e.g., hypertension, diabetes, atrial fibrillation) should be managed to achieve maximum risk reduction for recurrent stroke [Evidence Level A] as these are associated with cognitive impairment [Evidence Level B].  Refer to the CSBPR Secondary Prevention of Stroke module for additional information.
    1. Treatment of hypertension may reduce cognitive decline, even in the absence of stroke events and should be addressed for all people with elevated blood pressure who are either at high risk [Evidence Level B] or have already experienced a stroke [Evidence Level A]. 
  2. Interventions for cognitive impairment should be tailored according to the following considerations:
    1. Goals should be person-centered and sensitive to the values and expectations of the person with stroke, their family and caregivers [Evidence Level B]. 
    2. Goals and interventions should take into account the strengths and weaknesses of the affected person’s cognitive profile and communication abilities [Evidence Level C].
    3. People with stroke and with communication and/or cognitive issues may require additional support (e.g., family involvement) to optimize participation in goal-setting and/or engagement in rehabilitation [Evidence Level C].
    4. Interventions should be individualized, based on best available evidence, and have the long-term aim to facilitate resumption of desired activities and participation (e.g., self-care, home and financial management, leisure, driving, return to work) [Evidence Level C]. 
    5. Severity of impairments: If the level of impairment has reached the moderate dementia stage (when the person is unable to live independently), it is reasonable for interventions to be more focused on providing education and support for the caregiver in addition to, or in lieu of, cognitive rehabilitation with the affected person (Evidence Level C].
  3. Interventions that may be considered for rehabilitation for vascular cognitive impairment may include compensation strategies and direct remediation/cognitive skill training [Evidence Level B]. The choice of strategies should be individualized to the person’s clinical profile. 
    1. Compensation strategy training should focus on teaching strategies to manage impairments and is often directed at specific activity limitations to promote independence [Evidence Level B]. It can include changes in the physical and or social environment or changing the way one performs an activity [Evidence Level B]. 
    2. Direct remediation/cognitive skill training should focus on providing intensive specific training to directly improve the impaired cognitive domain. It can include drill and practice exercises, mnemonic strategies (e.g., acronyms, songs), or computer or tablet-based tools directed at specific deficits [Evidence Level B].
  4. Memory impairments may be treated with compensation using external strategies (e.g. assistive electronic and non-electronic devices) and using internal strategies (e.g., encoding and retrieval strategies, self-efficacy training and errorless learning), with some evidence for benefits to activity limitations [Evidence Level B].
    1. Targeted computerized skill training directed by a therapist may be considered for working memory deficits [Evidence Level B]
  5. Executive function deficits may be treated with meta cognitive strategy training and/or formal problem-solving strategies, under the supervision of a trained therapist [Evidence Level B].
  6. Internal strategy training may be considered and includes strategies to improve goal management, problem solving, time management, and metacognitive reasoning [Evidence Level B].
  7. Aerobic exercise can be considered as an adjunct therapy for cognitive impairment including attention, memory and executive function [Evidence Level B].  Refer to CSBPR Stroke Rehabilitation module for additional information on exercise.
  8. People who have experienced a stroke with cognitive impairment and evidence of changes in mood (e.g., depression, anxiety), or other behavioural changes on screening could be referred to and managed by an appropriate mental healthcare professional [Evidence Level B].  Refer to Section Two Part One on post-stroke depression for additional information.

Clinical Consideration for Management of Vascular Cognitive Impairment

  1. The learning abilities of people with vascular cognitive impairment following stroke should be considered when determining the intervention, and how best to provide education to maximize benefits of the intervention (e.g. teach tasks using demonstration, verbal instruction, slow pace and repetition as needed).
  2. Computer based interventions may be considered as an adjunct to clinician-guided treatment – research in this area continues to evolve rapidly.
  3. Evidence for impact on activity or participation limitations is limited and requires more research. 
  4. Emerging cognitive interventions that may be of potential benefit include repetitive transcranial magnetic stimulation or transcranial direct current stimulation, the use of virtual reality environments, and application of constraint-induced approaches for the impaired cognitive domain.  These strategies require more research before recommendations can be developed on their use.

Refer to CSBPR Stroke Rehabilitation module for additional information related to treatment of other domains, including communication, visual-perceptual disorders and neglect in people who have experienced a stroke and vascular cognitive impairment.

2.4 Pharmacotherapy for Vascular Cognitive Impairment following Stroke
  1. For people with evidence of vascular cognitive impairment following stroke, a referral to a healthcare professional or team with expertise in vascular cognitive impairment may be considered for further assessment and recommendations regarding pharmacotherapy [Evidence Level C].
  2. Cholinesterase inhibitors (donepezil, rivastigmine and galantamine) and the N-methyl-D-aspartate (NMDA) receptor antagonist memantine may be considered in individual persons with vascular or mixed dementia following stroke, based on randomized trials showing small magnitude benefits in cognitive outcomes [Evidence Level A].  Refer to Clinical Consideration iv below for additional information.

Note: These medications are currently approved by Health Canada for the treatment of Alzheimer’s Disease.  They have not received approval for the indication of vascular cognitive impairment.

Clinical Considerations related to Pharmacotherapy for Vascular Cognitive Impairment

  1. It should be noted that most of the available evidence is based on people who meet the criteria for vascular dementia or mixed dementia. Thus, evidence for pharmacological treatment effects in vascular cognitive impairment is limited at this time.
  2. Severity of cognitive impairment should be considered in decisions for pharmacological management. 
  3. People demonstrating vascular cognitive impairment following stroke may be susceptible to adverse events given the frequent presence of medical comorbidities and concomitant medications.
  4. The clinical relevance of benefits of cholinesterase inhibitors (donepezil, rivastigmine and galantamine) and the N-methyl-D-aspartate (NMDA) receptor antagonist memantine remains controversial particularly in view of the risk of adverse events and a potential increased risk of mortality; therefore, the use of these medications should be based on clinical judgment that small improvements in cognition would have a meaningful impact on the quality of life of the person following stroke.
Rationale +-

Vascular cognitive impairment affects up to 60 percent of people who have had a stroke 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 (Teasell 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, visualized as lacunes or white matter hyperintensities on T2-weighted images, are common 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. 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 support services over the long term. 

In most population studies, vascular dementia is the second most common cause of dementia, after Alzheimer disease, although recent evidence especially from imaging studies (PURE-MIND, SPRINT-MIND) has demonstrated the significant presence of vascular changes in many more dementia cases than previously understood.  A single macroscopic hemispheric infarct is sufficient to cause dementia in people with intermediate Alzheimer pathology.  Further, vascular cognitive impairment has been associated with several heart health issues including heart failure, atrial fibrillation, and congenital heart defects, and these comorbidities are also associated with increased risk of stroke.

System Implications +-
  1. Public education to increase awareness that cognitive changes may be considered as manifestations of vascular disease and stroke. 
  2. Public education to increase awareness of untreated or uncontrolled hypertension and other vascular risk factors and their relationship to cognitive changes and dementia.
  3. Professional education to increase awareness among family physicians and primary care health professionals that people who have experienced a stroke with vascular risk factors, if not treated, will be at high risk for cognitive deficits, even in the absence of overt stroke.
  4. Professional education across specialties (e.g., nephrology, ophthalmology, family medicine) to increase awareness that people with small-vessel disease should be investigated for stroke risk factors and cognitive impairment.
  5. Access to interprofessional teams with the expertise to appropriately manage people with vascular cognitive impairment across the continuum of stroke care and in the community.
  6. The development and implementation of an equitable and universal pharmacare program, implemented in partnership with the provinces, designed to improve access to cost-effective medicines for all people in Canada regardless of geography, age, or ability to pay. This program should include a robust common formulary for which the public payer is the first payer.
  7. Mechanisms to ensure good communication and information flow between the range of specialists and programs beyond the core stroke care providers to meet the varied needs of individuals post stroke (e.g., mental health specialists, cognitive specialists, geriatric programs).
  8. Continuing professional education to ensure proficiency in screening and assessment administration, interpretation and management of people who have experienced a stroke demonstrating post stroke and vascular cognitive impairment or at risk of vascular cognitive impairment. 
Performance Measures +-
  1. Percentage of people with stroke or stroke risk factors who undergo 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. Proportion of people with stroke and possible cognitive changes detected during screening, who are referred for more in-depth cognitive or neuropsychological assessment at transition points and setting changes across 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. Proportion of people who experience a stroke who are subsequently diagnosed with vascular cognitive impairment at one, three, six, and twelve months following index stroke event.
  4. Percentage of family/caregivers who received education on people who have experienced a stroke’s current cognitive functioning including recommendations that consider the person’s best ability to function in the least restrictive environment.

Measurement notes

  • Recommendations for vascular cognitive impairment 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 documentation.
Summary of the Evidence +-

Vascular Cognitive Impairment Evidence Tables and Reference List

  1. Evidence Table 2A Vascular Cognitive Impairment: Screening and Assessment 
  2. Evidence Table 2B Vascular Cognitive Impairment: Cognitive Rehabilitation 
  3. Evidence Table 2C Vascular Cognitive Impairment: Pharmacological Therapy  

Prevalence and Screening

It has been estimated that 5% of all people over the age of 65 years, in Canada, have evidence of vascular cognitive impairment. Vascular cognitive impairment refers to cognitive impairment due to all forms of cerebral vascular disease, including stroke, with severity that ranges from mild cognitive impairment to dementia (Gorelick et al. 2011). However, the reported vascular cognitive impairment prevalence tends to be higher in individuals who have experienced a stroke, with values ranging from 20.4% to 22% within the first three months of stroke (Douri et al. 2013, Bejot et al. 2011), to 29% over five years (Pendlebury et al. 2015). Lower estimates have also been reported. Swartz et al. (2017) found the prevalence of moderate-severe cognitive impairment was 14% in a group of patients attending a stroke prevention clinic, when screened using a 10-item version of the Montreal Cognitive Assessment test (MoCA), which was incorporated into their Depression, Obstructive Sleep Apnea, Cognitive Impairment (DOC) screening tool, developed to screen for obstructive sleep apnea (DOC-apnea), depression (DOC-mood) and cognitive impairment (DOC-Cog), using a single instrument. Estimates of the prevalence of VCI will vary depending on the screening tool used to identify VCI, the setting of the screening (e.g. community clinic, outpatient rehabilitation clinic), and the stage of stroke recovery. For example, among stroke survivors, the prevalence of any cognitive impairment 10 years post stroke was quite different, depending on the screening tool used. Using the Mini-Mental State Exam (MMSE), the prevalence was 45.7% compared with 61.5%, using MoCA criteria (Delavaran et al. 2016). 

In a systematic review including 73 studies, Pendlebury and Rothwell (2009) reported that the prevalence of dementia was at least doubled following recurrent stroke compared with first-ever stroke and was higher in hospital-based vs. community-based studies. At three to six months, post-stroke incidence of dementia was approximately 20%, which increased linearly at a rate of 3.0% in hospital-based studies of either first or recurrent stroke. The most commonly reported predictors of post-stroke dementia were older age, lower education level, previous stroke, diabetes, atrial fibrillation, pre-existing cognitive impairment and stroke severity. The authors suggested 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. 

The most commonly used tests for the screening of cognitive function post stroke are the MoCA and the MMSE. Detailed descriptions of these and other screening tests used in stroke populations can be found in Table 2B (see appendix two). The sensitivities and specificities of the MMSE to identify mild cognitive impairment at cut-points <26/27 have been estimated at 82% and 76%, respectively (Cumming et al. 2013), and to detect dementia or multidomain cognitive impairment, 88% and 62%, respectively (Lees et al. 2014). In contrast, the corresponding estimates of sensitivity and specificity for MoCA at a cut-point of <26 were 84% and 45% (Lees et al. 2014). Overall, the MoCA appears more sensitive to the presence of VCI compared to the MMSE, particularly with mild deficits (e.g., Pendlebury et al. 2012, Godefroy et al. 2011, Toglia et al. 2011, Dong et al. 2010), although equivalence has been noted in other studies, notably with patients of moderate to severe strokes (Dong et al. 2012).    

Vascular Risk Factor Reduction

The use of antihypertensive agents following stroke has been evaluated in a limited number of trials in which cognition was the primary, and not one of the secondary outcomes. The most recent of these trials, Prevention of Decline in Cognition after Stroke Trial’ (PODCAST, Bath et al. 2017), included 83 participants who were functionally independent, and had sustained a stroke in the previous three to seven months, were aged ≥70 years with telephone MMSE > 16, or aged > 60 years and t-MMSE 17 to 20 and with hypertension. Participants were randomized to an intensive blood pressure reduction group, or a guideline standard group, for at least six months. Although the trial was terminated before recruiting the 600 planned participants, intensive blood pressure management, which resulted in significant reductions in systolic and diastolic blood pressures, did not alter cognition outcomes in persons with normal or near-normal cognition at baseline. The dementia outcomes of the Memory and Cognition IN Decreased Hypertension (SPRINT-MIND), a sub group of SPRINT, which also evaluated the reduction in blood pressure on cognitive performance, will be released in 2019. Blood pressure reduction was one component of a multifaceted intervention program in the Austrian Polyintervention Study to Prevent Cognitive Decline After Ischemic Stroke (ASPIS) trial (Matz et al. 2015). Within three months of stroke, 202 patients were randomized to a 24- month intensive intervention program, emphasizing blood pressure control (goal of <140/90 mm Hg and <135/85 mm Hg for diabetics), increased physical activity (goal of moderate or vigorous, 3-5x/week), diet (elements of a prudent diet and Mediterranean type diet), while encouraging weight loss in the obese, cognitive training (home-based exercises) and cessation of smoking; or to a control group (n=101), which received care according to standard guidelines. At 24 months, there was no significant difference between groups in the number of patients who experienced cognitive decline (10.5% of patients in the intervention group vs. 12.0% in the control group).
Cognitive Rehabilitation 

Cognitive rehabilitation interventions for vascular cognitive impairment associated with stroke, focus on common deficits of attention, memory or executive function.  In general, interventions may be considered to have one of two objectives: 1) to reinforce or re-establish previous behavioural skills or function (e.g., to remediate with computerized exercises) or 2) to teach compensatory mechanisms (e.g., strategy training) that may be either internal or external to the individual (Cicerone 2011). Wentink et al. (2016) describes the effect of an enriched environment for persons with self-perceived cognitive impairments, 12–36 months after stroke. Participants engaged in a computer-based gaming activity for 600 minutes in total over eight weeks targeting five cognitive domains (attention, speed, memory, flexibility and problem solving). At the end of the treatment period, persons in the intervention group performed significantly better on measures of working memory, but not attention, compared with those in the control group who received weekly information about stroke from the study’s website. A Cochrane review (Loetscher & Lincoln, 2013) included the results of six RCTs evaluating interventions designed to either restore attentional functions or provide compensatory strategies for persons with attention deficits post stroke. Cognitive rehabilitation resulted in significantly greater improvement on assessments of divided attention, but not global attention function or functional outcome (activities of daily living). In a systematic review, Hoffman et al. (2010) also suggested that cognitive rehabilitation did not result in significant improvement in ability to perform ADLs or instrumental ADLs. Ten hours of teaching patients a strategy to compensate for mental slowness in real-life tasks was associated with significantly greater improvement in attention tasks in persons following a stroke, with onset of at least three months (Winkens et al. 2009). A systematic review by Cha & Kim (2013) evaluating the efficacy of computer-based cognitive rehabilitation revealed an overall effect size of 0.54 (medium effect) on attention outcomes, with similar results reported when used in the acute or chronic stage of stroke. 

In a recent Cochrane review, das Nair & Lincoln (2016) included the results of 13 RCTs (n=514) examining various memory rehabilitation strategies in persons with memory problems following stroke. Interventions included computerized memory training, strategy training, the use of external memory aides and imagery mnemonics. Memory training was associated with significant improvements in short-term subjective memory measures (SMD= 0.36, 95% CI 0.08-0.64, p=0.01), but not objective memory measures. Training was also not associated with long-term effects of either subjective or objective memory measures, assessed three to seven months following treatment. Memory self-efficacy training was reported to improve subjective daily memory reports and quality of life in one RCT with 153 stroke patients in the chronic phase of stroke (Aben et al., 2013), with benefits persisting at six and 14 months (Aben et al. 2014).  Cicerone et al. (2011) also recommend use of external aids to improve function directly (e.g., alarms, pagers, notebooks) for severe memory impairment following stroke or traumatic brain injury (TBI).

Evidence for the effectiveness of the rehabilitation of executive function and problem solving is less compelling. Rozental-Iluz et al. (2016) reported no significant differences between groups in mean scores of The Executive Function Performance Test following three months of participation in an interactive video-game group intervention, compared with persons randomized to a traditional group intervention for motor recovery at least six months post stroke. A Cochrane review (Chung et al. 2013) included the results of 19 RCTs of persons with stroke and other acquired brain injuries. Thirteen trials examined strategies restoring components of executive function (restorative and compensative interventions). No significant treatment effects were reported with respect to concept formation, planning, flexibility, working memory, or extended ADLs between intervention and control groups. Poulin et al. (2012) included 10 studies examining cognitive rehabilitation strategies to remediate executive function impairments. Nine studies examined an intervention provided during the chronic phase of care.  The authors concluded that there is limited evidence to suggest that problem-solving strategies and paging systems are associated with significant improvement in performance on functional tasks that involve executive control, compared to no treatment.

Physical activity may also be beneficial for the rehabilitation of cognitive impairment post stroke. Oberlin et al. (2017) included the results of 14 RCTs and reported a small to moderate mean effect size (Hedges’ g =0.304, 95% CI 0.14–0.47, p<0.001). Cumming et al. (2012) included nine trials investigating the effect of exercise on cognition in stroke patients, also reported a significant, but small, pooled treatment effect (standardized mean difference = 0.2, 95%, CI 0.04 to 0.36, p=0.015). Other treatment modalities, including non-invasive brain stimulation using transcranial direct current stimulation (tDCS), virtual reality and music listening have also been associated with improvements in cognitive function following stroke (Yun et al. 2015, Kim et al. 2011, Sarkamo et al. 2008).


Cholinergic agents, including donepezil, rivastigmine and galantamine have been used in the treatment of dementia of the Alzheimer’s type and vascular dementia. The usefulness of these agents has also been investigated in the treatment of post-stroke cognitive deficits. Donepezil, a selective acetylcholinesterase inhibitor, has been the subject of three large randomized controlled trials (Black et al. 2003, Wilkinson et al. 2003, Roman et al. 2010). In all trials, patients with possible or probable dementia following stroke were randomized to receive 5 or 10 mg of the agent or placebo for 24 weeks. In all trials, participants in in the donepezil groups demonstrated significantly greater improvement on the Vascular Alzheimer’s Disease Assessment Scale cognitive subscale (V-ADAS-cog) or the Alzheimer’s Disease Assessment Scale cognitive subscale (ADAS-cog), compared with those in the placebo group. In one trial (Roman et al 2010) the risk of mortality was higher in the donepezil group (n=11/648) than the placebo group (n=0/326; p=0.02), but there were no mortality differences in two other trials and no significant difference when the results of all three trials were pooled. A Cochrane review including the results of three RCTs examined the use of rivastigmine for the treatment of vascular cognitive impairment, vascular dementia, or mixed dementia (Birks et al. 2013). Within this review, a single study (n=710) reported a significant treatment effect in favour of rivastigmine in cognitive response (change in Mini MMSE score: MD= 0.06, 95% CI 0.11 to 1.09, p=0.02, and change in Vascular Dementia Assessment Scale from baseline: MD= -1.3, 95% CI-2.62 to 0.02, p=0.05). No significant effects of treatment were reported for either of the other two trials. Treatment with 24 mg galantamine for 24 weeks was associated with significantly greater improvements in ADAS-cog scores compared with placebo in two trials that included patients with probable or possible post-stroke dementia (Auchus et al. 2007, Erkinjuntti et al. 2002).

The use of the MNDA receptor antagonist, memantine has also been reported to improve cognitive function in persons with vascular dementia. Orgogozo et al. (2002) and Wilcock et al. (2002) both randomized patients to receive 20 mg memantine daily or placebo for 28 weeks. Memantine was associated with significantly greater improvement on the ADAS-cog at the end of the study period in both trials, compared with placebo; however, there was no significant difference between groups in the proportion of patients rated as stable or improved based on the Clinician’s Interview-Based Impression of Change Plus Caregiver Input (60% versus 52%, p=0.23) (Orgogozo et al. 2002), nor was there a significant difference in the Clinician Global Impression of Change between groups (Wilcock et al. 2002). 

Other pharmacological agents have been evaluated in the treatment of post-stroke dementia. Citicoline was associated with higher odds of being dementia free among persons recovering from first-ever ischemic stroke with persistent neurological deficit (Alvarez-Sabin et al. 2013). Antidepressants have also been associated with improvements in executive function (Narushima et al. 2007) and problem solving (Jorge et al. 2010) in persons recovering from stroke. The use of Actovegin, a novel therapeutic agent, which may enhance oxidative metabolism in the brain was recently evaluated in persons following acute ischemic stroke and Montreal Cognitive Assessment test score of ≤25 points (Guekht et al. 2017). The mean decreases from baseline in ADAS-cog+ scores at six and 12 months were significantly greater for persons in the Actovegin group. At three, six and 12 months, significantly more patients in the Actovegin group met the definition of responder (≥4-point improvement in ADAS-cog subscore from baseline).

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