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Section 7.4

Vascular cognitive impairment and dementia

All patients with vascular risk factors and those with clinically evident stroke or transient ischemic attack should be considered at high risk for vascular cognitive impairment.

Patients considered at high risk for cognitive and perceptual impairment are those with vascular risk factors such as hypertension, age > 65, hyperlipidemia, diabetes, clinical stroke, neuroimaging findings of covert stroke or white matter disease, hypertension-associated damage to other target organs, and/or those patients with cognitive or functional changes that are clinically evident or reported during history-taking.

7.4.1   Assessment

  1. All high-risk patients should be screened for cognitive impairment using a validated screening tool [Evidence Level B].
  2. Screening to investigate a person’s cognitive status should address arousal, alertness, attention, orientation, memory, language, agnosia, visuospatial/perceptual function, praxis and executive functions such as insight, judgment, social cognition, problem- solving, abstract reasoning, initiation, planning and organization [Evidence Level C].
  3. The Montreal Cognitive Assessment is considered more sensitive to cognitive impairment than the Mini Mental Status Exam in patients with vascular cognitive impairment. Its use is recommended when vascular cognitive impairment is suspected [Evidence Level B].17
    Additional validation is needed for the Montreal Cognitive Assessment as well as other potential screening instruments such as the 5-minute protocol from the Vascular Cognitive Impairment Harmonization recommendations.
  4. Post-stroke patients should also be screened for depression, since depression has been found to contribute to cognitive impairment in stroke patients. A validated screening tool for depression should be used [Evidence Level B].17
    Refer to recommendation 7.3 for additional information
  5. Post-stroke patients who have cognitive impairment detected on a screening test should receive additional cognitive and/or neuropsychologic assessments as appropriate to further guide management [Evidence Level B].17

7.4.2   Timing

  1. All patients considered at high risk for cognitive impairment should be assessed periodically as indicated by 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. Those who have had a transient ischemic attack or stroke should be assessed using a validated screening tool and, where indicated, undergo a more in-depth assessment of cognitive and perceptual status at various transition points throughout the continuum of stroke care [Evidence Level C]. Transition points may include:
    1. during presentation to emergency when cognitive, perceptual or functional concerns are noted
    2. upon admission to acute care, particularly if any evidence of delirium is noted
    3. upon discharge home from acute care or during early rehabilitation if transferred to inpatient rehabilitation setting
    4. periodically during in-patient rehabilitation stage according to client progress and to assist with discharge planning
    5. periodically following discharge to the community by the most appropriate community healthcare provider according to client’s needs, progress and current goals.

7.4.3   Management

  1. All vascular risk factors should be managed aggressively to achieve optimal control [Evidence Level A].
    Refer to section 2 for additional information
  2. Patients who demonstrate cognitive impairments in the screening process should be referred to a healthcare professional with specific expertise in this area for additional cognitive, perceptual and/or functional assessments [Evidence Level B].
    1. Additional assessments should be undertaken to determine the severity of impairment and impact of deficits on function and safety in activities of daily living and instrumental activities of daily living, and to implement appropriate remedial, compensatory and/or adaptive intervention strategies [Evidence Level B].
    2. A team approach is recommended, and healthcare professionals may include an occupational therapist, neuropsychologist, psychiatrist, neurologist, geriatrician, speech-language pathologist or social worker [Evidence Level C].
  3. An individualized, patient-centred approach should be considered to facilitate resumption of desired activities such as return to work, leisure, driving, volunteer participation, financial management, home management and other instrumental activities of daily living [Evidence Level C].17
  4. Intervention strategies including rehabilitation should be tailored according to the cognitive impairments and functional limitations as well as remaining cognitive abilities, as identified through in-depth assessment and developed in relation to patients’ and caregivers’ needs and goals [Evidence Level B].
  5. Strategy training provides individuals who have limitations in activities of daily living with compensatory strategies to promote independence and should be offered to patients with cognitive challenges. [Evidence Level B]. The evidence for the effectiveness of specific interventions for cognitive impairment in stroke is limited and requires more research.
    1. Attention training may have a positive effect on specific, targeted outcomes and should be implemented with appropriate patients [Evidence Level C].
    2. Compensatory strategies can be used to improve memory outcomes [Evidence Level B]
  6. Patients with evidence of depression or anxiety on screening should be referred and managed by an appropriate health professional [Evidence Level C].
    Refer to recommendation 6.2 for additional information    .
  7. Pharmacotherapy
    1. Patients with evidence of vascular cognitive impairment should be referred to 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 Nerosciences (AIREN) diagnostic criteria [Evidence Level B].17
    3. 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].
    4. There is fair evidence of small magnitude benefits for donepezil in cognitive and global outcomes, with less robust benefits on functional measures. Donepezil can be considered a treatment option for vascular dementia [Evidence Level B].

 

    Rationale

    Vascular cognitive impairment affects up to 60 percent of stroke survivors and is associated with decreased function in activities of daily living and instrumental activities of daily living. Patients may require long-term, ongoing intervention and/or rehabilitation.28, 575 It has been suggested that cognitive abilities such as abstract thinking, judgment, short-term memory, comprehension and orientation are important in predicting functional status at discharge.28In 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 higher mortality (61 percent versus 25 percent).576

    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.576 Evidence is emerging that demonstrates that for every clinically evident stroke, there are six to nine so-called “covert” strokes. Signs of covert stroke are often manifested as cognitive impairment signs and symptoms.28 Intracerebral small-vessel disease is a significant issue that is on the rise with the aging of the population, leading to an increase in the need for long-term care support services.

    In most population studies, vascular dementia is the second most common cause of dementia, after Alzheimer disease. 576 The combination of Alzheimer disease and vascular disease results in the commonest substrate of dementia in the elderly. A single macroscopic hemispheral infarct is sufficient to cause dementia in people with intermediate Alzheimer pathology.

    System Implications
    • Education of the public on adding cognitive changes to the signs and symptoms of stroke.
    • Professional education across specialties (e.g., nephrology, ophthalmology) to increase awareness that patients with small-vessel disease should be investigated for stroke risk factors and cognitive impairment.
    • Ongoing professional education to ensure proficiency in assessment administration, interpretation and management of cognitive impairment.
    • Increased awareness among family physicians that patients with vascular risk factors, if not treated, will be at high risk for cognitive deficits.
    • Increased professional education and awareness for primary care practitioners regarding small-vessel disease and vascular cognitive impairment.
    • Increased public awareness programs focused on untreated hypertension and other vascular risk factors and their relationship to dementia.
    Performance Measures
    1. Percentage of patients with stroke who undergo a brief cognitive screening at each transition point along the continuum of stroke care (i.e., acute inpatient care, inpatient rehabilitation, outpatient and ambulatory clinics, and stroke prevention clinics) in the community following inpatient discharge and at any time when there is a suspected change in the patient’s cognitive status.
    2. Percentage of patients with stroke who are referred for more in-depth cognitive or neuropsychologic assessment during inpatient care, inpatient rehabilitation, outpatient and ambulatory clinics (stroke prevention clinics) and/or following inpatient discharge to the community.
    3. Percentage improvement in control of high blood pressure and other vascular risk factors in patients with vascular cognitive impairment.

    Measurement Notes

    • This is a new area and will require a great deal of education for healthcare professionals especially in the area of documentation.
    Summary of the Evidence

    Vascular cognitive impairment represents a spectrum of cognitive disorders associated with stroke and cerebrovascular disease ranging in severity from vascular cognitive impairment without dementia to vascular dementia. As noted in the Evidence-Based Review of Stroke Rehabilitation, as many as two-thirds of patients experience cognitive impairment or decline following stroke and approximately one-quarter to one-third develop dementia.28Nyenhuis and Gorelick reported that more than 700 000 strokes occur annually in the United States.577 Vascular cognitive impairment affects up to half of stroke survivors and represents a substantial public health burden, with 1998 per-patient care costs estimated to be US$9313 for persons with mild disease and US$21 399 for persons with severe disease. Vascular cognitive impairment is also associated with reduced life expectancy and impaired daily functional abilities. For instance, Teasell and collaborators28 further noted that mortality rates among stroke patients with dementia were two to six times greater than among patients without dementia. In terms of factors affecting recovery, Newman and associates conducted a post hoc analysis of longitudinal data (n = 3680) and found that diabetes, HDL and homocysteine predicted poorer cognitive function and greater disability after stroke for this sample population.578

    Pendlebury and Rothwell conducted a systematic review of the prevalence, incidence and associated factors for pre-stroke and post-stroke dementia.579The review included 22 hospital-based and eight population-based eligible cohorts (7511 patients) described in 73 papers. The pooled prevalence of pre-stroke dementia was higher (14.4%, 95% CI 12.0—16.8) in hospital-based studies than in population-based studies (9.1%, 6.9—11.3). Although post-stroke (≤1 year) dementia rates were heterogeneous overall, the rates ranged from 7.4% (4.8—10.0) in population-based studies of first-ever stroke in which pre-stroke dementia was excluded to 41.3% (29.6—53.1) in hospital-based studies of recurrent stroke in which pre-stroke dementia was included. The cumulative incidence of dementia after the first year was little greater (3.0%, 1.3 – 4.7) per year in hospital-based studies than expected on the basis of recurrent stroke alone. Medial temporal lobe atrophy, female sex, and a family history of dementia were strongly associated with pre-stroke dementia, whereas the characteristics and complications of the stroke and the presence of multiple lesions in time and place were more strongly associated with post-stroke dementia. They report that the estimates of the prevalence of dementia are consistent: 10 percent of patients had dementia before first stroke, 10 percent developed new dementia soon after first stroke, and more than a third had dementia after recurrent stroke. Further, the strong association of post-stroke dementia with multiple strokes and the prognostic value of other stroke characteristics highlight the central causal role of stroke itself as opposed to the underlying vascular risk factors. Therefore, they conclude that there is a likely effect of optimum acute stroke care and secondary prevention in reducing the burden of dementia.

    After stroke, vascular cognitive impairment can be found in many cognitive domains. Common deficits are seen in attention, memory, executive function, language, visuospatial processing and speed of processing in both the acute and rehabilitation phases580, 581and can remain chronic in the long-term. 582-586 Hoffmann reported that the frequency of higher cortical function abnormality (aphasia, apraxia, amnesia and executive dysfunction) based on bedside neurologic testing was 63.5 percent in 1000 patients within the first month after stroke. 587 High rates have been found in other studies using neuropsychologic testing two–three months after stroke as well.575, 588These deficits persist in the chronic phase after stroke; in one study examining cognitive recovery from three to 27.7 months, most patients showed no improvement or declined.306 Likewise, Tatemichi and coworkers found that 35 percent of a group of 227 patients showed cognitive impairment on multiple tests at 3 months after stroke, with improvement seen in only 12 percent of patients in memory, orientation, visuospatial function and attention in yearly follow-ups.589

    More information about cognitive deficits in the early phase after stroke is needed, however, to accurately estimate early cognitive recovery. The degree of cognitive recovery after stroke may be underestimated when the baseline examination is performed at three months after stroke (after spontaneous recovery has already occurred).590 Van Zandvoort and associates attempted to describe the feasibility and validity of neuropsychologic evaluation in the early stage following a stroke event, examining consecutive stroke patients four to 20 days following their first ischemic stroke (n = 57).591 At the early stage of evaluation, 77 percent of patients were able to successfully complete 82 percent of the tasks required of them. Cognitive impairment in many stroke survivors remains evident in the chronic phase and constitutes a significant issue for rehabilitation and long-term management.

    The impact of cognitive impairment on rehabilitation and long-term functional outcome has been documented widely. The presence of cognitive impairment in general is associated with increased functional disability and poor outcome.589, 592, 593 Poor outcome has been specifically associated with spatial neglect and related symptoms, such as anosognosia.594-598 Attention and memory deficits also affect outcome, as well as executive dysfunction.583, 599-604 Cognitive deficits may also adversely affect physical disability via reduced skill reacquisition in physical rehabilitation.601, 605, 606

    One-quarter to one-third of stroke patients develop dementia. In a UK-based population study of 4075 individuals aged 65 and over (Medical Research Council Cognitive Function and Ageing Study),607 stroke was significantly associated with an increasing risk for the development of dementia, and Kalaria and Ballard found that post-stroke dementia occurs in up to 30 percent of stroke patients.608 The risk for developing dementia may be up to 10 times greater among individuals with stroke than for those without.28 Independent risk factors for poorer recovery and the development of dementia following stroke include increasing age, lower levels of formal education and nonwhite race.

    While the risk of vascular cognitive impairment is high in stroke populations, vascular cognitive impairment is also frequent in the general elderly population. According to the Canadian Study of Health and Aging (CSHA), it is estimated that five percent of all people over the age of 65 years have evidence of vascular cognitive impairment (using the inclusive concept of vascular cognitive impairment, no dementia; vascular dementia; and mixed Alzheimer and cerebrovascular disease).609 In forty-four percent of the subgroup with vascular cognitive impairment, no dementia developed dementia over a five-year period.610 The underlying causal factors for development of dementia are mixed. Elderly people with silent brain infarcts and white matter lesions are at a strongly increased risk of stroke, which cannot be explained by the major stroke risk factors.611 Vascular dementia is the second most common cause of dementia after Alzheimer disease, in the order of 20 percent. Population autopsy studies, however, suggest that while pure vascular dementia is less frequent (< 10 percent of cases), combined cerebrovascular disease and Alzheimer disease is the most common neuropathologic finding.576, 612 Vascular dementia may be the second leading cause of late-life dementia in the United States and Europe, and is a leading cause of dementia in countries where stroke rates are high, such as Japan and other countries in the Far East.613

    Thus, there is increasing recognition of the impact of vascular disease on cognitive impairment and the need for assessment and management. In the National Institute of Neurological Disorders and Stroke – Canadian Stroke Network Vascular Cognitive Impairment Harmonization Standards, Hachinski and colleagues made recommendations for an abbreviated clinical examination focusing on vascular impairment. It was advised that this evaluation should include an assessment with respect to cognitive impairment and vascular contribution. 614

    Instruments are needed that are reliable at detecting changes in cognitive function following stroke. The Mini Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA) are both frequently used in clinical practice. Pendlebury and colleagues conducted a study comparing these two measurement tools during the six month and five year follow-up visits as part of the Oxford Vascular Study.615Of 493 patients seen in follow-up, 413 (84%) were testable. Untestable patients were older (75.5 versus 69.9 years, P􏰀r2􏰅0.80, P􏰀PP􏰅