Seizures after cerebrovascular events: Risk factors and clinical features

BackgroundEpileptic seizures are well known sequelae of patients with stroke but only little is known about the different risk factors and about the influence of the different types of stroke including sinus thrombosis and bleedings on developing such seizures. Further, the association of post-stroke seizures and conventional vascular risk factors has not been evaluated to date.MethodsWe performed a cohort study on a sample of 593 consecutive patients with different types of cerebrovascular events. In 421 patients, sufficient data were obtained in a personal interview over a mean observation period of 30 months. Data regarding the clinical history were recorded from the patients’ charts.ResultsThe total prevalence of epileptic seizures was 11.6%, the total annual risk was 4.6%. We detected the following significant risk factors: younger age at stroke; higher NIH stroke scale score; any coagulopathy. TIA was found significantly less frequent as a cause of seizures as compared to infarction, bleeding, and sinus thrombosis. Patients with bleeding (14.3%) and with sinus thrombosis (16.3%) were significantly more frequent in the seizure group than in the non-seizure group (6.7% and 1.6%, respectively). The location of stroke, including cortical versus subcortical, did not influence the risk of seizures. The majority of patients developed secondary generalized seizures (57.1%). In adjusted analyses, the two major risk factors for post-stroke epilepsy were a higher NIH stroke scale and a sinus thrombosis as the initial cerebrovascular event. Common lifestyle, vascular, and metabolic risk factors of stroke and for dementia were not associated with the development of seizures.ConclusionsIn conclusion, our data show that epileptic seizures occur in particular after major strokes and in sinus thrombosis. Interestingly, conventional vascular risk factors were not associated with the occurrence of post-stroke seizures. Considering the risk for seizures after certain types of cerebrovascular events might help to early identify patients for anticonvulsive treatment. In the future, it should be investigated whether these patients might benefit from pre-emptive anticonvulsant treatment.     

Why are stroke patients prone to develop dementia?

Stroke patients are more likely to develop dementia than age- and sex-matched controls but the pathogenesis of dementia remains unresolved in most of them. The aim of this review is to determine, from the available literature, the theoretical reasons for a stroke patient to become demented. We found three distinct factors that may explain the occurrence of dementia after a stroke. Firstly, post-stroke dementia may be the direct consequence of the vascular lesions of the brain: this is the most likely cause in patients with normal cognitive functions before a strategic infarct, especially in young patients, in Icelandic-type hereditary amyloid angiopathy and in cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy. Secondly, post-stroke dementia may be due to an associated asymptomatic Alzheimer pathology; the reasons for such an association are that (1) some cases of dementia occurring after a stroke are progressive and Alzheimer’s disease (AD) is the most frequent cause of progressive dementia; (2) age and APOE ɛ 4 genotype are risk factors for both AD and ischaemic stroke; (3) a vasculopathy is often associated with AD. Lastly, white matter changes may also contribute to dementia because they often indicate small-vessel disease and a higher risk of stroke recurrence, and may lead to slight cognitive impairment. Finally, the summation of vascular lesions of the brain, white matter changes, and Alzheimer pathology might lead to dementia, even when each type of lesion, on its own, is not severe enough to induce dementia. Therefore, in patients followed up after a stroke, the term “post-stroke dementia” is probably more appropriate than that of vascular dementia because it includes all possible causal factors. Received: 15 July 1996 Accepted: 19 October 1996     

Working status is related to post stroke/TIA cognitive decline: data from the TABASCO study

Background and AimsOccupational status may influence physical and mental post-stroke outcomes. We aimed to evaluate the association between occupational status and type, or engagement in social and family activities, neuroimaging measures and cognitive decline (CD) in a prospective cohort of stroke patients.MethodsWe included 273 first-ever stroke survivors at working age. All patients underwent 3T MRI at admission, as well as clinical and cognitive assessments at admission, 6, 12 and 24 months thereafter.ResultsNinty nine (36.3%) of the participants were unemployed prior to the stroke. Age, sex, work type, other comorbidities, stroke severity or location were not associated with return to work. Patients who returned to work (87.4%) had better cognitive results and less depressive symptoms than those who retired after the event.Pre-stroke unemployment was associated with diabetes mellitus, hypertension, dyslipidemia, depression, poorer cognitive scores and brain atrophy. During the follow-up, 11% developed CD. CD was more common among previously unemployed than employed participants (19.2% vs. 6.3%, p = 0.001). Multiple regression adjusted for risk factors, revealed that pre-stroke unemployment was an independent predictor of CD (HR, 3.0; 95% CI: 1.06–8.44). Furthermore, engagement in mentally stimulating jobs decreased the risk for CD.ConclusionsPre-stroke unemployment and post-stroke work disruption were each associated with depression and poorer cognitive performance up to two years post-stroke, as well as with brain atrophy at admission. Retirement after the stroke may increase the risk of developing CD. These results highlight the importance of continued employment in preserving cognitive abilities among stroke survivors.     

Pre-stroke sleep duration and post-stroke depression

ObjectiveSleep disturbance and depression are common in stroke patients, however, little is known about the role of sleep in post-stroke depression. This study examined the association between pre-stroke sleep duration and depression at 90 days post-stroke in a population-based bi-ethnic sample.MethodsThe study included 1369 stroke patients from the Brain Attack Surveillance in Corpus Christi project who survived 90 days post-stroke. Depression at 90 days post-stroke was assessed by the 8-item Patient Health Questionnaire, and pre-stroke sleep duration was self-reported shortly after stroke in reference to the pre-stroke state. Multiple imputation and inverse probability weighting were used to deal with missing data and attrition. Weighted logistic regression models were fit to examine the association between pre-stroke sleep duration and post-stroke depression.ResultsThe mean age was 68.2 years, and 63.6% were Mexican American. The prevalence of post-stroke depression was highest among participants reporting less than 6 hours of sleep before stroke (52.4%, 95% confidence interval = 45.7%–59.0%). Compared with participants reporting 7–8 hours of sleep before stroke, those with short sleep duration had significantly increased odds for post-stroke depression (odds ratio = 1.96; 95% confidence interval = 1.38–2.79), after adjustment for sociodemographic, stroke and pre-stroke characteristics including pre-stroke depression.ConclusionsPre-stroke short sleep duration may be an independent risk factor for post-stroke depression.     

Processing of emotional words after stroke: An electrophysiological study

ObjectiveAuditory evoked potentials (EP) were used to examine the neural processing of personal–emotional and neutral words, in a group of 14 people with post-stroke aphasia and an equal sized control group to determine whether the EP differed between groups and word types.MethodsEffects of the emotional value of the words and participant group were assessed on EP. Latencies and amplitudes of EP were analyzed for the two groups (aphasia and control) in response to word type (emotional and neutral).ResultsN1 amplitudes were smaller and P2 and P3 were delayed in the aphasia group, for both word types, indicating effects of stroke on processing of both neutral and emotional words. P3 amplitudes were larger for emotional words in both groups. These differences in late cortical responses between word types for both groups suggest distinct neural networks involved in the response to emotional and neutral words, even with post-stroke language impairment.ConclusionsThe neurophysiological processing of affective speech in aphasia has been revealed. This opens up the interpretation of these results to the critical assessment and therapeutic identification of emotional language in people with aphasia.SignificanceThis study has implications not just for aphasia but allows for further exploration of other neurological conditions.     

Plasma Pro-Enkephalin A and Ischemic Stroke Risk: The Reasons for Geographic and Racial Differences in Stroke Cohort

ObjectivesThe opioid neuropeptide pro-enkephalin A (PENK-A) may be a circulating marker of cardiovascular risk, with prior findings relevant to heart failure, kidney disease, and vascular dementia. Despite these findings, the association of PENK-A with ischemic stroke is unknown, so we examined this association in a prospective cohort study and analyzed differences by race and sex.Materials and MethodsThe REasons for Geographic and Racial Differences in Stroke study (REGARDS) is a prospective cohort study of 30,239 Black and White adults. Plasma PENK-A was measured in 473 participants that developed first-time ischemic stroke over 5.9 years and 899 randomly selected participants. Cox models adjusted for demographics and stroke risk factors were used to calculate hazard ratios (HRs) of stroke by baseline PENK-A.ResultsPENK-A was higher with increasing age, female sex, White race, lower body mass index, and antihypertensive medication use. Each SD higher increment of PENK-A was associated with an adjusted HR of 1.20 (95% CI 1.01-1.42) for stroke, with minimal confounding by stroke risk factors. Spline plots suggested a U-shaped relationship, particularly in White men, with an adjusted HR 3.88 (95% CI 1.94-7.77) for the 95^th versus 50^th percentile of PENK-A in White men.ConclusionsHigher baseline plasma PENK-A was independently associated with future stroke risk in REGARDS. This association was most apparent among White men. There was little confounding by established stroke risk factors, suggesting a possible causal role in stroke etiology. Further research is needed to understand the role of endogenous opioids in stroke pathogenesis.     

Risk factors and mechanisms of post-stroke dementia]

Stroke significantly increases the risk of dementia in subjects aged 55 years or more. Twenty to 25 p. 100 of patients are demented 5 years after a stroke. Age and supratentorial location of the vascular lesion are risk factors for post-stroke dementia. Volume, left side of the lesion, large middle cerebral artery infarction, lesions of the frontal lobe, second stroke, diabetes, aphasia, clinical features expressing the severity of the stroke event in the acute phase, mitral valve prolapse, atrial fibrillation, depression, concomitant hypoxic/ischemic disorders, and white matter changes have also been found as predictors of dementia. There are many different mechanisms of vascular pathology that may lead to dementia: ischemic or hemorrhagic lesions, large vessel disease including multi-infarct and strategic single infarct, small-vessel disease including lacunes and white matter changes, hypoperfusion.... Post-stroke dementia may not be due only to vascular lesion. Some post-stroke dementias have a progressive onset and course. The cognitive decline may pre-exist to the stroke, even when a dementia is not diagnosed. This suggests a degenerative process. Alzheimer's disease is frequent in ages when the majority of strokes occur. Alzheimer's and vascular diseases share common risk factors such as age, APOE4, hypertension, and smoking. Patients with low MMS scores and AD patients are at risk for stroke. Moreover, white matter changes are associated with stroke and Alzheimer's disease and may contribute to the cognitive decline. Many post-stroke dementias could be multifactorial. Even when vascular lesions and degenerative changes (mainly Alzheimer changes) are not severe enough, no their own, to be the cause of dementia, their summation may reduce the preclinical stage of the degenerative process.     

Pre-stroke habitual prolonged sleep as a predictor for post-stroke sleep quality,stroke-related quality of life,and lifestyle values

BackgroundProlonged sleep is a higher stroke risk, but post-stroke prolonged sleep facilitates stroke recovery. No study has explored the relationship between pre- and post-stroke prolonged sleep and their involvement in stroke-related quality of life (QOL). This study aimed to clarify the role of pre- and post-stroke prolonged sleep in QOL and sleep quality during hospitalization.MethodsFifty-one subacute stroke inpatients were enrolled. QOL was assessed by the Stroke and Aphasia QOL Scale-39-J. Sleep quality and lifestyle values were assessed by original questionnaires.ResultsPatients in pre-stroke prolonged sleep > 8 h had a higher incidence of post-stroke poor sleep quality than those belonging to the normal or shorter hours (OR 5.33, 95% CI 1.30–21.84, p = 0.047). In addition, pre-stroke prolonged sleep was associated with lower scores of psychosocial QOL and lifestyle values of “accepting disability; caring about what other people think of what you do”. In contrast, post-stroke prolonged sleep was associated with the lower risk of post-stroke poor sleep quality (OR 0.27, 95% CI 0.08–0.86, p = 0.045). Post-stroke high sleep quality had higher (better) scores of physical and energy QOL, and lifestyle values of “caring about what other people think of what you do; having some places to go out after discharge” compared with post-stroke poor sleep quality. Post-stroke prolonged sleep was derived from pre-stroke not prolonged sleep rather than pre-stroke prolonged sleep (p = 0.039, Chi-square test).ConclusionsPre-stroke prolonged sleep is associated with a higher incidence of post-stroke poor sleep quality and lower scores of QOL and lifestyle values after stroke.     

Sex differences in sleep-disordered breathing after stroke: results from the BASIC project

Objective/BackgroundSleep-disordered breathing (SDB), an independent risk factor for stroke, is associated with worse post-stroke outcomes. Differences in the relationship between SDB and stroke may exist for women versus men. In this population-based study, we compared the prevalence of both pre- and post-stroke SDB by sex. We also explored whether menopausal status is related to post-stroke SDB.Patients/MethodsWe performed a cross-sectional study of subjects enrolled in the Brain Attack Surveillance in Corpus Christi (BASIC) project. Each subject (n = 1815) underwent a baseline interview including the Berlin Questionnaire to assess pre-stroke SDB risk and, if relevant, questions regarding menopausal status. Subjects were offered overnight SDB screening with a validated portable respiratory device (n = 832 with complete data). Log Poisson and linear regression models were used to assess the differences in SDB between men and women with adjustment for demographics, stroke risk factors, stroke severity, and other potential confounders.ResultsWomen were less likely than men to be at high risk for pre-stroke SDB (56.6% versus 61.9%) (prevalence ratio [PR] 0.87 for women; 95% confidence interval [CI], 0.81–0.95). A lower proportion of women than men (50.8% versus 70.2%) had post-stroke SDB by respiratory monitoring (PR 0.71; 95% CI, 0.63–0.80). SDB severity was higher for men than for women (mean difference in respiratory event index [REI] 6.5; 95% CI, 4.3–8.7). No significant association existed between post-stroke SDB and either menopausal status or age at menopause.ConclusionsAfter acute ischemic stroke, SDB was more prevalent and more severe in men than in women.     

Physical activity in vascular cognitive impairment: Systematic review with meta-analysis

BackgroundVascular cognitive impairment (VCI) is the second most common cause of cognitive impairment worldwide and includes a spectrum from vascular cognitive impairment no dementia (VCIND) to vascular dementia (VaD). There is no specific pharmacological treatment approved for VCI. Physical activity has been indicated to be a promising preventive measure for cognition, with direct as indirectly benefits, while improving several modifiable vascular risk factors, so potentially effective when considering VCI. Our aim was to conduct a systematic review with a meta-analysis approaching the potential preventive role of physical activity on VCI.MethodsA systematic search was conducted in 7 databases. A total of 6786 studies were screened and assessed for eligibility, culminating in the inclusion of 9 observational prospective studies assessing physical activity impact irrespectively the type for quality assessment and qualitative and quantitative synthesis. Quantitative synthesis was performed using the reported adjusted HRs. Physical activity was handled as a dichotomous variable, with two groups created (high versus low physical activity). Subgroup analyses were done for risk of bias, VaD and length of follow-up.ResultsThere was considerable methodological heterogeneity across studies. Only three studies reported significant associations. The overall effect was statistically significant (HR 0.68, 95%CI 0.54-0.86, I² 6.8%), with higher levels of physical activity associated with a smaller risk of VCI overtime, particularly VaD.ConclusionsThese findings suggest that physical activity is a potential preventive factor for vascular dementia. Insufficient data is available on VCIND. Randomized studies are desired to confirm these results.     

Cognitive ability in young adulthood and risk of dementia in a cohort of Danish men,brothers, and twins

IntroductionWe examined the association between cognitive ability in young adulthood and dementia in Danish men, brothers, and male twins.MethodsIn total, 666,986 men born between 1939 and 1959 were identified for dementia diagnosis in national registries from 1969 to 2016. The association between cognitive ability from draft board examination and dementia was examined using Cox regression.ResultsDuring a 44-year follow-up, 6416 (0.96%) men developed dementia, 1760 (0.26%) and 970 (0.15%) of which were classified as Alzheimer's and vascular dementia, respectively. Low cognitive ability was associated with increased risk of dementia (hazard ratio [HR]_{per SD decrease} 1.33 [95% confidence interval {CI} = 1.30–1.35]) with the strongest associations for vascular dementia (HR_{per SD decrease} 1.47 [95% CI = 1.31–1.56]) and a weaker for Alzheimer's disease (HR_{per SD decrease} 1.07 [95% CI = 1.03–1.13]). The intrabrother and twin analyses (taking shared family factors into account) showed attenuated risk estimates but with wide CIs.DiscussionLow early-life cognitive ability increases the risk of dementia before the age of 78 years. The association is partly explained by shared family factors.     

Predictors of depressive symptoms in patients with stroke – a three-month follow-up

Background and purposeDepression is one of the most common post-stroke complications, which could impair rehabilitation outcome and quality of life, and could also increase mortality after stroke. The aim of the present study was to assess the association between demographic, socioeconomic and clinical (stroke risk factors, type of stroke, location of vascular lesion, cognitive functions) factors on the presence and severity of post-stroke depressive symptoms in patients after first ever stroke as well as on their social functioning.Material and methodsA prospective, cohort study with a three-month observation period was performed in seven centres. Severity of depressive symptoms was assessed with the help of a short, 15-item version of the Geriatric Depression Scale (GDS), 3 months after stroke onset.ResultsOn the basis of GDS (GDS ≤ 5 points or > 5 points) patients were allocated to a group without (n = 160) or with symptoms suggestive of depression (n = 82). The study groups did not differ with respect to age, sex or place of residence. Univariate logistic regression analysis showed that independent predictors for the presence of symptoms suggestive of depression at 3 months after stroke were: low level of education, low income, greater severity of stroke, worse functional status, self-reported problems with daily-living activities and need of help in daily living activities. More than 60% of patients with depressive symptoms limited their social contacts. Patients with depressive symptoms were unsatisfied with their relations with life partners and friends.ConclusionsOur study showed a complex aetiology of post-stroke depressive symptoms with an important role of socioeconomic factors. Depressive symptoms after stroke worsen existing health, social and economic problems, and cause social isolation of patients.     

Incident depression and mortality among people with different types of dementia: results from a longitudinal cohort study

Purpose

The aim of this study was to investigate the independent and combined association of incident depression and dementia with mortality and to explore whether the magnitude of the association varies according to different types of dementia, including Alzheimer’s disease and vascular dementia.

Methods and design

The study was based on a population-based longitudinal cohort consisting of 9940 participants at baseline and followed for over 14 years. The sample used for the analyses included 6114 participants with available information on diagnosis of incident dementia and depression. For survival analyses, Cox regression models with incident dementia (n = 293; 5%) and incident depression (n = 746; 12%) as time-dependent variables were used.

Results

Cox models adjusted for relevant confounders indicated that comorbidity of incident vascular dementia and incident depression was associated with a much higher mortality risk (HR 6.99; 95% CI 3.84–12.75) than vascular dementia in the absence of depression (HR 2.80; 95% CI 1.92–4.08). In contrast, estimates for comorbidity of Alzheimer’s disease and depression were slightly lower than those for Alzheimer in absence of depression (HR 3.56; 95% CI 1.83–6.92 and HR 4.19; 95% CI 2.97–5.90, respectively). Incident depression in the absence of incident dementia was only weakly associated with mortality.

Conclusions

These findings indicate that depression and vascular dementia might have synergistic effects on mortality. The results have relevant public health implications for prevention, routine screening for and early treatment of depression among older people, especially those at risk of vascular dementia.

     

The measure of stroke environment (MOSE): development and validation of the MOSE in post-stroke populations with and without aphasia

Objectives. The purpose of this paper is to present the development and psychometric properties of a new environmental measure that identifies barriers and facilitators in receptivity, physical environment and communication for post-stroke populations, including survivors with aphasia.

Methods. The Measure of Stroke Environment (MOSE) was developed using information from semi-structured interviews and three pilot studies. Reliability and validity were assessed in 43 post-stroke participants.

Results. The MOSE contains 47 items across 33 questions in three domains (receptivity, physical environment, communication). Internal consistency reliability was high (.83 to .85) across each domain and over the entire assessment (.91). Convergent validity showed moderate correlation with the Stroke Impact Scale (.33 to .37), the National Institute of Health Stroke Scale (-.31 to -.46) and the Boston Diagnostic Aphasia Examination (.55 to .61). Persons with aphasia had significantly lower scores on the communication domain. Stroke survivors with (26% overall difficulty) and without aphasia (31% overall difficulty) continue to experience difficulty ≥ 2 years post-stroke.

Discussion. The MOSE offers a brief, reliable and valid assessment of environmental barriers and facilitators to participation for post-stroke survivors reintegrating into their communities. Stroke survivors with very mild deficits continue to experience barriers from the environment many years post-stroke. These barriers are not typically identified during the rehabilitation process but persist post-reintegration.

Conclusion. The MOSE is able to determine how frequently a stroke survivor faces challenges in their environment and how that impacts his or her participation.     

Effect on anxiety and depression of a multifactorial risk factor intervention program after stroke and TIA: a randomized controlled trial

Objectives: Depression and anxiety related to stroke are caused by vascular lesions and psychological reactions. Treatment of vascular and modifiable behavioral risk factors reduces the risk of stroke and may also reduce the risk of emotional changes after stroke. We aimed to investigate whether a multifactorial risk factor intervention program in patients with first-ever stroke or transient ischemic attack (TIA) can influence post-stroke anxiety and depressive symptoms in patients one year post-stroke.

Method: The study population consisted of first-ever stroke and TIA patients allocated in a randomized, evaluator-blinded, controlled trial to care as usual or a structured and multidisciplinary follow-up including intensive treatment of vascular risk. The primary endpoint (cognition) has previously been reported. The secondary endpoint, reported here, was changes in the Hospital Anxiety and Depression Scale (HADS) from baseline to 12-month follow-up.

Results: One hundred and ninety-five patients were randomized. The estimated difference between treatment groups, in changes in HADS, from baseline to 12 months was ?1.32 (95% confidence interval: ?2.61, ?0.04; P = 0.044) in favor of the intervention group. One year post-stroke, 4/85 (4.7%) patients in the intervention group and 12/89 (13.5%) in the control group suffered from depression (P = 0.045), while 7/85 (8.2%) patients in the intervention group and 13/89 (14.6%) patients in the control group suffered from anxiety (P = 0.19).

Conclusion: A structured, multidisciplinary, multifactorial risk factor program including vascular risk factor management may be associated with reduced HADS scores and a lower prevalence of depressive symptoms one year after stroke.     

Do Acetylcholinesterase Inhibitors Prevent or Delay Psychotropic Prescribing in People With Dementia? Analyses of the Swedish Dementia Registry

ObjectivesTo investigate whether acetylcholinesterase inhibitor (AChEI) use prevents or delays subsequent initiation of psychotropic medications in people with Alzheimer's disease (AD) and Lewy body dementia (LBD).MethodsCohort study of 17,763 people with AD and LBD, without prior psychotropic use at time of dementia diagnosis, registered in the Swedish Dementia Registry from 2007 to 2015. Propensity score-matched regression models were used to compute hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between time-dependent AChEI use and risk of psychotropic initiation.ResultsCompared with matched comparators, AChEI users had a lower risk of antipsychotic (HR: 0.85, 95%CI: 0.75–0.95) and anxiolytic (HR: 0.76, 95%CI: 0.72–0.80) initiation. In subanalyses, this association remained significant at higher AChEI doses, and in AD but not LBD. There were no associations between AChEI use and initiation of antidepressants or hypnotics.ConclusionAChEI use may be associated with lower risk of antipsychotic and anxiolytic initiation in AD, particularly at higher doses. Further investigation into aceytylcholinesterase inhibitors in behavioral and psychological symptoms of dementia management in LBD is warranted.     

卒中类型、卒中部位与卒中后癫痫的多因素关系

目的探讨卒中类型、卒中部位与卒中后癫痫的多因素关系,为卒中后癫痫的防治提供参考。方法以1804例卒中患者为研究对象,收集其性别、年龄、卒中类型、卒中部位、卒中后癫痫发生的时间等资料,根据卒中后是否发生癫痫,将患者分为卒中后无癫痫组(n=1487)和卒中后癫痫组(n=317),分析卒中后癫痫发作的危险因素。结果共317例卒中后癫痫发作患者,其中早发性癫痫141例(44.48%),迟发性癫痫176例(55.52%)。不同卒中部位及卒中类型的癫痫发病率为17.57%。多因素logistic回归分析显示,卒中部位中的顶叶合并蛛网膜下腔、额叶合并颞叶、额叶合并颞叶和枕叶、单一颞叶是卒中后发生癫痫的危险因素(P<0.01),其中单一颞叶是卒中后早发性癫痫的危险因素(P<0.01)。脑梗死患者常见早发性癫痫(23.66%),脑出血患者常见迟发性癫痫(47.95%)。结论卒中类型中的脑梗死、脑出血、蛛网膜下腔出血与卒中后癫痫有关;卒中部位中顶叶合并蛛网膜下腔、额叶合并颞叶、额叶合并颞叶和枕叶、单一颞叶与卒中后癫痫有关。     

Aphasia As a Predictor of Stroke Outcome

Purpose of Review

Aphasia is a common feature of stroke, affecting 21–38% of acute stroke patients and an estimated 1 million stroke survivors. Although stroke, as a syndrome, is the leading cause of disability in the USA, less is known about the independent impact of aphasia on stroke outcomes.

Recent Findings

During the acute stroke period, aphasia has been found to increase length of stay, inpatient complications, overall neurological disability, mortality, and to alter discharge disposition. Outcomes during the sub-acute and chronic stroke periods show that aphasia is associated with lower Functional Independence Measures (FIM) scores, longer stays in rehabilitation settings, poorer function in activities of daily living, and mortality. Factors that complicate the analysis of aphasia on post-stroke outcomes, however, include widely different systems of care across international settings that result in varying admission patterns to acute stroke units, allowable length of stays based on reimbursement, and criteria for rehabilitation placement.

Summary

Aphasia arising from stroke is associated with worse outcomes both in the acute and chronic periods. Future research will have to incorporate disparate patterns in analytic models, and to take into account specific aphasia profiles and evolving methods of post-stroke speech-language therapy.

     

The role of subjective cognitive complaints and depressive symptoms in social re-integration following stroke: a mediation explanation in a cross-sectional sample

Background: For long-term stroke survivors, objective neuropsychological impairments and subjective cognitive difficulties are common, and may contribute to ongoing difficulties in community reintegration. However, subjective cognitive complaints have been as much associated with low mood as with actual cognitive performance.

Objective: The objective of our study was to investigate the extent to which subjective cognitive complaints predicted community reintegration following a stroke, and whether this relationship would be mediated by emotional status.

Methods: Using a cross-sectional design, patients with a primary diagnosis of stroke (n = 102; age range 25–89 years) were recruited from the register of a neurological rehabilitation service if they were at least 6 months post-stroke and had been discharged home following the stroke. Exclusions included history of dementia, co-morbid psychiatric or neurological disorder, or significant aphasia. Assessments included the Subjective Cognitive Complaints Questionnaire, the Community Integration Questionnaire, and the Depression Anxiety and Stress Scale.

Results: Subjective cognitive complaints were common, with moderate to high levels of complaint most frequent for working memory (58.9%), and information processing speed (53%). Subjective cognitive complaints were significantly associated with social integration (r = ?.23, p < .05). However, examination of relationships using statistical mediation revealed that depressive symptoms fully mediated the relationship between subjective cognitive complaints and social integration.

Conclusions: Subjective cognitive complaints are common in long-term outcome following stroke and predict difficulty in community reintegration. However, this relationship is mediated by variation in emotional status. Therefore, addressing cognitive complaints through cognitive rehabilitation programs that include components to improve mood (for example, building self-efficacy or confidence) may also improve community reintegration post-stroke.