2. Déficience cognitive vasculaire

Les déficits cognitifs d’origine vasculaire touchent jusqu’à 60 % des personnes ayant subi un AVC, et ils sont associés à un moins bon rétablissement et une fonction réduite dans les activités de la vie quotidienne et les activités instrumentales de la vie quotidienne. Les patients pourraient nécessiter une intervention et une réadaptation continues à long terme (Teasell et coll., 2009; Madureira et coll., 2001). Les capacités cognitives dans les domaines des fonctions exécutives, de l’attention et de la mémoire semblent importantes pour prédire l’état fonctionnel au moment du congé. En outre, les déficits cognitifs peuvent être chroniques et évolutifs après un AVC. Selon les estimations, la démence après un AVC survient à trois mois chez 26 % des patients victimes d’un AVC (intervalle de confiance à 95 %, 3 % parmi les témoins du même âge) et nuit au rétablissement. Les déficits cognitifs augmentent la dépendance à long terme et sont associés à un taux de mortalité accru (61 % comparativement à 25 %) (Black, 2007).

Les déficits cognitifs dus à une pathologie vasculaire silencieuse sont également en hausse. Les AVC silencieux, visualisés comme des lacunes ou des hyper signaux dans la substance blanche sur les images pondérées selon T2, sont fréquents et associés au déclin cognitif, à la démence et à l’AVC. Des données commencent à démontrer que, pour chaque AVC clinique évident, il pourrait y avoir jusqu’à 10 AVC silencieux. La maladie des petits vaisseaux intracérébraux est un trouble à la hausse avec le vieillissement de la population, menant à une augmentation du besoin de services de soutien à long terme. 

Dans la plupart des études de population, la démence vasculaire arrive au second rang parmi les causes de démence après la maladie d’Alzheimer, bien que des données récentes, principalement des études d’imagerie (PURE-MIND, SPRINT-MIND), ont démontré la présence significative de modifications vasculaires dans un plus grand nombre de cas de démence que ce que l’on croyait. Un seul infarctus hémisphérique macroscopique est suffisant pour causer la démence chez des personnes manifestant la pathologie d’Alzheimer intermédiaire. De plus, les déficits cognitifs d’origine vasculaire ont été associés à plusieurs maladies du cœur, comme l’insuffisance cardiaque, la fibrillation auriculaire et les cardiopathies congénitales, et ces comorbidités sont également associées à un risque accru d’AVC.

1. Éducation du public afin d’accroître la sensibilisation au fait que les changements cognitifs peuvent être considérés comme des manifestations de la maladie vasculaire et de l’AVC. 
2. Éducation du public afin d’accroître la sensibilisation à une hypertension non traitée ou non maîtrisée et d’autres facteurs de risque cardiovasculaires et leur relation avec les changements cognitifs et la démence.
3. Éducation des professionnels afin d’accroître la sensibilisation parmi les médecins de famille et les fournisseurs de soins primaires au fait que les personnes qui ont subi un AVC et qui présentent des facteurs de risque cardiovasculaires, si elles ne sont pas traitées, augmenteront leur risque de déficits cognitifs, même en l’absence d’AVC manifestes.
4. Éducation des professionnels de toutes les spécialités (p. ex., néphrologie, ophtalmologie, médecine familiale) afin qu’ils soient plus sensibles au fait que les personnes présentant une maladie des petits vaisseaux doivent subir un dépistage des facteurs de risque de l’AVC et des déficits cognitifs.
5. Accès aux équipes interprofessionnelles possédant les compétences nécessaires pour gérer de façon appropriée dans le continuum de soins de l’AVC et dans la communauté des personnes atteintes de déficits cognitifs d’origine vasculaire.
6. Élaboration et mise en œuvre d’un régime d’assurance-médicaments équitable et universel, en partenariat avec les provinces, afin d’améliorer l’accès à des médicaments rentables pour toute la population, et ce, peu importe la situation géographique, l’âge ou le revenu. Ce programme doit comprendre une liste étoffée de médicaments admissibles pour laquelle l’État est le premier payeur.
7. Mécanismes permettant d’assurer une excellente communication et transmission d’informations entre les divers spécialistes et programmes au-delà du noyau de fournisseurs de soins de l’AVC, afin de répondre aux besoins variés des personnes victimes d’un AVC (p. ex., spécialistes en santé mentale, spécialistes de la cognition, programmes gériatriques).
8. Formation professionnelle continue pour s’assurer d’une exécution compétente de l’administration et de l’interprétation du dépistage et d’une évaluation, ainsi que la gestion des personnes présentant des déficits cognitifs après l’AVC et d’origine vasculaire, ou à risque de déficits cognitifs d’origine vasculaire.

1. Pourcentage de personnes victimes d’un AVC ou présentant des facteurs de risque d’AVC, qui sont soumises à un dépistage cognitif à chaque point de transition dans le continuum de soins de l’AVC (c.-à-d., soins aigus hospitaliers, réadaptation en milieu hospitalier, cliniques extrahospitalières et de prévention de l’AVC) et dans la communauté après avoir obtenu leur congé de l’hôpital et à n’importe quel moment lorsqu’un changement dans l’état cognitif est soupçonné. (Indicateur de base)
2. Proportion des personnes ayant subi un AVC et ayant des changements cognitifs possibles détectés durant le dépistage, qui sont orientées vers une évaluation cognitive ou neuropsychologique aux points de transition et lors des changements de milieux dans le continuum de soins de l’AVC (par exemple, pendant les soins et la réadaptation à l’hôpital, dans les cliniques extrahospitalières et ambulatoires, ou dans le cadre d’un programme comme la clinique de prévention de l’AVC), et/ou après avoir reçu un congé de l’hôpital pour retourner dans la communauté.
3. Proportion des personnes qui ont subi un AVC ayant reçu un diagnostic de déficit cognitif d’origine vasculaire un mois, trois mois, six mois et douze mois après l’AVC de référence.
4. Pourcentage de membres de la famille et d’aidants ayant reçu une formation sur la fonction cognitive actuelle des personnes qui ont subi un AVC, qui comprend des recommandations sur la capacité de fonctionner de la personne au meilleur de son habileté dans un milieu le moins restrictif possible.

Notes sur la mesure des indicateurs

• Les recommandations pour les DCV et les indicateurs de rendement correspondants s’appliquent au continuum de soins de l’AVC et doivent être prises en considération dans le contexte des soins hospitaliers, de la réadaptation en milieu hospitalier, des cliniques extrahospitalières, des services à domicile, et des cliniques de prévention de l’AVC, et/ou après le congé de l’hôpital pour retourner dans la communauté.

• En utilisant ces indicateurs de rendement, il est important de consigner le moment et le contexte (continuum de soins) des mesures prises. Les données sur les indicateurs sont disponibles en vérifiant les dossiers primaires. La qualité des données dépendra de la qualité de la documentation obtenue par les professionnels de la santé.

• Il s’agit d’un nouveau domaine qui exigera une importante éducation des professionnels de la santé, surtout en ce qui concerne la documentation.

Renseignements à l’intention des professionnels de la santé

• Tableau 2A : Critères de diagnostic pour les déficits cognitifs d’origine vasculaire et la démence 
• Tableau 2B : Résumé d’outils sélectionnés de dépistage et d’évaluation initiale des déficits cognitifs d’origine vasculaire chez les patients victimes d’un AVC.
• Lignes directrices d’harmonisation vasculaire (en anglais)
• Examen fondé sur les données probantes des troubles cognitifs et de l’apraxie (EBRSR) (en anglais)
• Partenariat canadien pour le rétablissement de l’AVC
• Énoncé scientifique de l’AHA/ASA sur les contributions d’origine vasculaire aux déficits cognitifs et à la démence (en anglais)
• Soins psychologiques après un AVC du NHS (en anglais)
• Trousse d’ergothérapie pour l’évaluation de la cognition, de la Winnipeg Regional Health Authority (en anglais)

Information relative au patient

• Prendre en main son rétablissement : « Guide du survivant selon les recommandations canadiennes pour les pratiques optimales de soins de l’AVC »
• Votre cheminement après un accident vasculaire cérébrale
• Info AVC (en anglais)
• Partenariat canadien pour le rétablissement de l’AVC - La vie après un AVC
• Trucs et trouvailles sur les soins de l’AVC - Un guide pour les personnes soignant les victimes d’un AVC 
• Liste de contrôle POST-AVC

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).

Pharmacotherapy

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).