Silent Brain Infarction Research Articles

Prevalence of Cerebral Atherosclerosis among Patients with Metabolic Syndrome: A Case Control Study on Egyptian Subjects

Background: The metabolic syndrome (MetS) is a clustering of vascular risk factors that tend to increase the risk of occurrence of diabetes mellitus type 2 (DMT2), cardiovascular and cerebro-vascular ischemic events. The aim of the present study is to investigate the association of extra-cranial and intracranial arterial atherosclerosis as well as silent brain infarction (SBI) with MetS, thereby determining the potential cerebrovascular atherosclerotic risk of MetS in the Egyptian population. Methods: A case control study was conducted on 50 Egyptian subjects with MetS and 30 without with age range from 40 - 60 years old. All participants were free from cerebrovascular ischemic events [stroke or transient ischemic attack (TIA)]. All participants underwent complete neurological examination, assessment of the diagnostic criteria for MetS, carotid and transcranial duplex ultrasonography (U/S) and brain MRI. Results: Preclinical carotid atherosclerosis (athero-sclerotic plaques with <50% stenosis) was associated with MetS (P value = 0.02) that persisted after adjustment for age and other confounders. There was no significant association between increased intima media thickness (IMT) and MetS. There was non-significant association between MetS and intracranial atherosclerotic disease (ICAD) or the degree of intracranial stenosis (ICS). Conversely, there was a highly significant association between MetS and SBI even after adjustment for age and other confounders (P value = 0.001). Conclusion: Metabolic syndrome is an important factor associated with mild to moderate atherosclerosis (<50% stenosis) and silent brain infarcts among asymptomatic individuals. Interventions to reduce MetS are important for prevention of subclinical and clinical cerebral atherosclerotic disease.

Concepts and opportunities for repair in cerebral microvascular disease and white matter stroke.

Diffuse changes in white matter resulting from cerebral microvascular disease contribute to cognitive impairment (Jokinen et al., 2011), declines in global functionality (Inzitari et al., 2009), and even death (Debette and Markus, 2010). Twenty years ago, estimations of the clinical incidence of cerebral microvascular disease approached 11 million per year in the US alone (Leary and Saver, 2003). More recent estimations suggest the prevalence of diffuse white matter disease and silent brain infarction approaches 20% and increases dramatically in the presence of cardiovascular risk factors (Fanning et al., 2014). Two common clinical presentations of cerebral microvascular disease include diffuse lesions resulting in T2/FLAIR signal abnormality on MRI scans throughout the white matter. Highly related to this diffuse form, is the classic lacunar infarction, with imaging evidence suggesting that new infarcts occur at the leading edge of prior T2/FLAIR signal abnormality (Duering et al., 2013), with subtle changes in axonal diffusivity occurring in the same region (Maillard et al., 2011). Cellular events within this white matter penumbral region are therefore a likely contributor to the progressive nature of white matter disease. Despite the growing prevalence of cerebral microvascular disease, there are no known efficacious treatment strategies to prevent the progression or repair the injury burden of ischemic white matter lesions. In part, this results from a comparative lack of understanding about the precise pathophysiology of cerebral microvascular disease nor the resultant cellular biology that underlies diffuse or focal changes in white matter. This lack of understanding exists because of limitations on the ability to appropriately model white matter lesions in an easily accessible animal model such as the mouse. With the recent development of several variations in a mouse model of focal white matter stroke (Nunez et al., 2016), the field is poised for significant advances in understanding the cellular mechanisms underlying white matter lesions resulting from cerebral microvascular disease and to identify leading strategies to repair ischemic white matter lesions. Here, we outline the neurobiologic concepts and major strategies for repair of diffuse cerebral microvascular disease and white matter stroke (Figure 1).

Dilated Virchow–Robin Spaces in First-Ever Lacunar Stroke Patients: Topography and Clinical Correlations

Dilated Virchow-Robin spaces (dVRSs) were regarded as a phenotype of cerebral small-vessel disease (SVD). However, the clinical correlations of dVRS were still unclear. In this study, we aimed to investigate the topography and clinical correlations of dVRS in first-ever lacunar stroke patients. Patients with first-ever lacunar stroke were recruited and had magnetic resonance scans to identify the presence and degree of dVRS in the basal ganglia (BG-dVRS), dVRS in the central semiovale (CSO-dVRS), leukoaraiosis, and silent brain infarction (SBI). The neurological deficits after stroke onset and functional outcome after 1 year were evaluated using National Institutes of Health Stroke Scale (NIHSS) and modified Rankin Scale, respectively. Clinical and radiological features were compared between patients with high and low degrees of dVRS, and between patients with favorable and unfavorable outcomes. Logistic regression models were constructed to identify the risk factors of unfavorable outcome. The NIHSS scores were not statistically different between patients with high and low degrees of dVRS. More patients with high degrees of BG-dVRS had unfavorable outcomes than those with low degrees of BG-dVRS. Logistic regression showed that the degrees of BG-dVRS, leukoaraiosis, and SBIs were not independent risk factors for the unfavorable outcome, whereas the total burden of SVD was an independent risk factor for the unfavorable outcome. The degrees of either BG-dVRS or CSO-dVRS were not associated with the severity of first lacunar stroke. BG-dVRS was related to the unfavorable 1-year outcome. This association might be based on the total severity of SVD.

Abstract 14839: Association of Silent Brain Infarction With CHADS2 Score and Left Atrial Abnormalities in Patients With Nonvalvular Atrial Fibrillation

Introduction: The CHADS2 score is widely used for risk stratification of thromboembolism in patients with nonvalvular atrial fibrillation (NVAF). Furthermore, LA abnormalities detected by transesophageal echocardiography (TEE) are also well known risk factors for thromboembolism in NVAF patients. On the other hand, silent brain infarction (SBI) relates to subsequent symptomatic brain infarction; however little is known regarding association among CHADS2 score, TEE parameters and SBI. Methods: The study population consisted of 103 neurologically asymptomatic patients with NVAF (mean age 63 ± 10 years) who underwent TEE. All participating patients underwent brain MRI and were calculated CHADS2 score. SBI was defined as an area of hypointense lesions that measured &gt;3 mm on T1-weighted images and hyperintense lesions on T2-weighted images by brain magnetic resonance imaging (MRI). LA abnormalities were defined as LA thrombus, spontaneous echo contrast, or low LA appendage emptying velocity (&lt;20 cm/s) detected by TEE. Results: Of 103 patients, 31 (30%) showed SBI on brain MRI. Over all mean CHADS2 score was 1.1 ± 0.9, and LA abnormalities were detected in 24 patients by TEE (23%). Mean CHADS2 score in patients with SBI was significantly higher than that in patients without SBI (P&lt;0.05). The prevalence of SBI increased along with increases in CHADS2 score (CHADS2 score of 0, 1, 2 and 3-6 in 13%, 23%, 47% and 80%, respectively, P&lt;0.05). Patients with SBI had a higher prevalence of LA abnormalities than those without SBI (P&lt;0.05). In patients with SBI with CHADS2 score of 0-1, LA abnormalities were detected in 5 of 14 patients (36%). Conclusions: In this study, both CHADS2 score and prevalence of LA abnormalities by TEE were higher in patients with SBI on MRI. LA abnormalities detected by TEE may discriminate risk for SBI even in patients with low CHADS2 score.

Interarm differences in systolic blood pressure and the risk of dementia and subclinical brain injury

IntroductionThis study examined whether interarm differences in systolic blood pressure (IDSBP) ≥10 mm Hg were associated with the risk of incident dementia and subclinical brain injury. MethodsBetween 1992 and 1998, 2063 participants of the Framingham Heart Study underwent assessment of IDSBP with results related to the 10-year risk of incident dementia including clinically characterized Alzheimer's disease. Secondary outcomes included markers of subclinical brain injury on magnetic resonance imaging. ResultsHigh IDSBP were associated with a greater risk of incident dementia (hazard ratio [HR] 1.92; 95% confidence interval [CI], 1.09–3.40) and Alzheimer's disease (HR, 2.32; 95% CI, 1.29–4.18), but only in those who carried an apolipoprotein E (APOE) ε4 allele. IDSBP also predicted lower total brain volumes and more prevalent silent brain infarcts in those who were APOE ε4 positive. DiscussionHigh IDSBP were associated with an increased risk of dementia, including clinical Alzheimer's disease, and subclinical brain injury in those who were APOE ε4 positive.

N-glycome Profile Levels Relate to Silent Brain Infarcts in a Cohort of Hypertensives.

BackgroundSilent brain infarcts (SBIs) are highly prevalent in the aged population and relate to the occurrence of further stroke and dementia. Serum N‐glycome levels have been previously associated with aging and they might be related as well to the presence of SBIs and age‐related white matter hyperintensities.Methods and ResultsWe determined the serum N‐glycome profile in a cohort study comprising 972 subjects and evaluated the relationship between N‐glycome levels and the presence and number of SBIs and with age‐related white matter hyperintensities grades, assessed by brain magnetic resonance imaging. Decreasing concentrations of bigalacto core‐α‐1,6‐fucosylated biantennary glycan and increasing concentrations of branching α‐1,3‐fucosylated triantennary glycan remained as independent predictors of SBIs (odds ratio 0.4, 95% CI 0.3–0.7 and odds ratio 1.8, 95% CI 1–3.2, respectively), after controlling for the presence of age and classic vascular risk factors. A similar pattern was found to be related to an increasing number of SBIs and white matter hyperintensities grade.ConclusionsN‐glycome levels might be potentially useful as biomarkers for the presence of silent cerebrovascular disease.

Vascular Cognitive Impairment

The term vascular cognitive impairment (VCI) has been proposed to encompass all people with cognitive impairment of cerebrovascular origin. VCI is not a single condition, but has several clinical presentations, etiologies, and treatment. VCI forms a spectrum that includes vascular dementia, mixed Alzheimer's disease with a vascular component, and VCI that does not meet dementia criteria. Multiple pathophysiological mechanisms contribute to VCI, accounting for its heterogeneity. Although main changes in the brain in VCI include cerebral infarcts, vascular cognitive impairment is thought to be due to factors beyond acute infarcts. Cerebral white matter lesions and silent brain infarcts are considered to be risk factors for VCI. The prevalence of VCI is high and this entity is poised to become the silent epidemic of the 21st century. Cognitive impairment due to cerebrovascular disease can to some extent be improved, and VCI prevented, if vascular risk factors are brought under control and strokes do not recur. Therefore, strategies that focus on the prevention and treatment of the cognitive impairment associated with cerebrovascular disease are high priority healthcare objectives.

Sonolysis in Prevention of Brain Infarction During Carotid Endarterectomy and Stenting (SONOBUSTER): a randomized, controlled trial.

Previous case series have detected silent brain infarctions in as many as one-third of patients after carotid endarterectomy (CEA) and in up to two-thirds of patients after carotid angioplasty and stenting (CAS). Sonolysis employs ultrasound to facilitate disruption of thrombi and has been shown to be safe and effective for improving long-term outcomes following acute stroke. Here, we examined whether intraoperative sonolysis alters the risk of new brain ischaemic lesions during CEA or CAS. All consecutive patients with internal carotid stenosis ≥70% indicated for CEA/CAS were screened in this prospective study. Patients were allocated randomly to sonolysis and control groups. Neurological examination, cognitive function tests, and brain magnetic resonance imaging (MRI) were conducted before intervention and at 24 and 30 days post-surgery. Of the 487 screened patients, 121 (87 males; mean age, 66.65 ± 7.17 years) were allocated to the sonolysis group and 121 (75; 66.02 ± 8.11 years) to the control group. New brain ischaemic lesions on post-procedure MRI were significantly less frequent in the sonolysis group than in the control group (31.4% of patients vs. 47.1%; P = 0.018). Sonolysis and CEA were identified as independent predictors of reduced brain ischaemic risk [sonolysis: odds ratio (OR) = 0.450 (0.215-0.942), P = 0.034and CEA: OR = 0.208 (0.087-0.495), P < 0.001]. Stroke or transient ischaemic attack occurred in one sonolysis patient and three control patients (P = 0.372). No significant group differences were found in post-intervention cognitive test scores (P > 0.3). This study provides Class II evidence that sonolysis during CEA or CAS reduces the risk of new brain ischaemic lesions. http://www.clinicaltrials.gov (NCT01591005).

Epidemiology of stroke in Finnish patients with Huntington's disease.

Diabetes mellitus and hypercholesterolemia are known risk factors of stroke, and altered glucose and cholesterol metabolism has been reported in patients with Huntington's disease (HD). We investigated the incidence and risk factors of stroke in this population. National registries were used to identify a cohort of 192 patients with HD. Data on stroke, silent cerebral infarcts and risk factors were obtained from the patient records. Five patients with an ischemic stroke (IS) were found suggesting a crude incidence of 42/100,000 person years. Silent brain infarcts were found in 13 patients and a hemorrhagic stroke in two patients, while none were found with a transient ischemic attack (TIA). The cumulative incidence of IS was 2.7% and that of silent cerebral infarct 6.7% by age of 65 years. The CAG age product (CAP) score, an estimate of genetic burden, was 495 ± 117 for the patients with IS or silent cerebral infarct and 568 ± 126 for the patients without ischemic events (P = 0.025 for difference). The frequency of diagnoses of stroke risk factors was at least twofold higher among the patients with IS or silent infarcts than among those without. Cerebrovascular disease is as common in patients with HD as in the general population, but minor cerebrovascular events and vascular risk factors may remain unrecognized. Genetic burden of the HTT mutation does not appear to increase the risk of stroke.

Bone Mineral Density is Negatively Associated with Arterial Stiffness in Men with Silent Brain Infarction

Bone Mineral Density is Negatively Associated with Arterial Stiffness in Men with Silent Brain Infarction

Acute Silent Brain Infarction in Monocular Visual Loss of Ischemic Origin

Background and Purpose: Non-arteritic branch/central retinal artery occlusions (BRAO/CRAO) and amaurosis fugax (AF) are predominantly caused by embolism. Additionally, transported embolic material could cause ischemic stroke. The aim of the study was to investigate the prevalence, pattern and underlying cause of concurrent acute brain infarctions in unselected patients with RAO and AF. Methods: A total of 213 consecutive patients with BRAO (20.7%), CRAO (47.4%), or AF (31.9%) were retrospectively studied from 2008 to 2013. Magnetic resonance imaging (MRI) was used to detect acute brain infarctions and a cardiovascular workup was performed to detect underlying etiologies according to the Trial of Org 10172 in Acute Stroke Management (TOAST). Results: MRI was obtained after 23.78 (±32.26) hours from the time of symptom onset. Acute brain infarctions were detected in 49 patients (23%); 44 of them (89.8%) did not experience any additional neurological symptoms. Older age (p < 0.001/p < 0.001), hypertension (p = 0.01/p = 0.03), atrial fibrillation (p = 0.006/p = 0.03) and type of RAO (p = 0.02/p = 0.016) were associated with total/silent stroke, respectively. In multivariate analysis, only age and type of occlusion remained positive predictors for silent stroke. Etiology of BRAO/CRAO and AF remained undetermined in 124 patients (58.2%). This rate was lower in patients with acute stroke (40.8 vs. 63.4%). Conclusions: Silent brain infarction is a frequent finding in unselected patients with BRAO/CRAO and AF. Etiology remains undetermined in approximately every second case. Because silent brain infarctions bear a high risk of future stroke, patients with BRAO/CRAO and AF should undergo prompt neuroimaging and cardiovascular checkup, preferably on a stroke unit.

Stroke in sickle cell disease

Sickle cell disease (SCD) is the second commonest cause of stroke in the pediatric population. Cerebrovascular complications in SCD may involve large or small vessels and present as large infarctions, intracranial or subarachnoid hemorrhage, moyamoya disease or silent infarcts. Predictors of stroke in SCD include high blood flow velocity on transcranial Doppler, low hemoglobin value, absence of alpha-thalassemia, high white cell count, hypertension, silent brain infarction, and a history of chest crisis. Regular blood transfusions are used for primary and secondary prevention of stroke in SCD. Other management strategies include stem cell transplantation,

Role of brain infarcts in behavioral variant frontotemporal dementia: Clinicopathological characterization in the National Alzheimer's Coordinating Center database

Diagnosing behavioral variant frontotemporal dementia (bvFTD) in patients with prior history of stroke or with silent brain infarcts on neuroimaging studies can be challenging. Vascular changes in patients with bvFTD are not unusual, but bvFTD tends to be ruled out in the presence of cerebrovascular disease. We aimed to identify the clinical, cognitive, and risk factor profile of bvFTD with coexistent cerebrovascular disease (V-bvFTD). We compared demographic data, clinical diagnoses, vascular risk factors, functional status, and normalized neuropsychological z-scores between patients with V-bvFTD versus bvFTD without concomitant cerebrovascular disease (NV-bvFTD) from the National Alzheimer's Coordinating Centre database. We included 391 neuropathologically-diagnosed cases of frontotemporal lobe degeneration. We excluded patients that were diagnosed with aphasic variants of frontotemporal dementia before death. Patients with V-bvFTD (n = 62) were older at the time of onset of cognitive decline (71.6 vs. 62.5 years, p < 0.001) and death (78.7 vs. 69.6, p < 0.001), more likely to be hypertensive (75.8% vs. 45.7%, p = 0.002) and to have a history of stroke (21.2% vs. 6.1%, p = 0.007) than those with NV-bvFTD (n = 329). V-bvFTD was often underdiagnosed, affected elderly patients, and had a similar cognitive profile as NV-bvFTD despite the presence of brain infarcts. In the whole cohort, we observed enhanced cognitive performance with increasing age quintiles despite larger proportions of cerebrovascular disease pathology, likely meaning that frontotemporal lobe degeneration–related primary neurodegeneration exerts a stronger impact on cognition than cerebrovascular disease. Coexisting cerebrovascular disease should not preclude the diagnosis of bvFTD.

Aberrant white matter networks mediate cognitive impairment in patients with silent lacunar infarcts in basal ganglia territory.

Silent lacunar infarcts, which are present in over 20% of healthy elderly individuals, are associated with subtle deficits in cognitive functions. However, it remains largely unclear how these silent brain infarcts lead to cognitive deficits and even dementia. Here, we used diffusion tensor imaging tractography and graph theory to examine the topological organization of white matter networks in 27 patients with silent lacunar infarcts in the basal ganglia territory and 30 healthy controls. A whole-brain white matter network was constructed for each subject, where the graph nodes represented brain regions and the edges represented interregional white matter tracts. Compared with the controls, the patients exhibited a significant reduction in local efficiency and global efficiency. In addition, a total of eighteen brain regions showed significantly reduced nodal efficiency in patients. Intriguingly, nodal efficiency-behavior associations were significantly different between the two groups. The present findings provide new aspects into our understanding of silent infarcts that even small lesions in subcortical brain regions may affect large-scale cortical white matter network, as such may be the link between subcortical silent infarcts and the associated cognitive impairments. Our findings highlight the need for network-level neuroimaging assessment and more medical care for individuals with silent subcortical infarcts.

Predictors of silent brain infarction on magnetic resonance imaging in patients with nonvalvular atrial fibrillation: A transesophageal echocardiographic study

Silent brain infarction (SBI) is often found in patients with atrial fibrillation (AF) and may be related to cognitive decline. We investigated the predictors of SBI on brain magnetic resonance imaging (MRI) using transesophageal echocardiography (TEE) in patients with nonvalvular AF. The study population consisted of 103 neurologically asymptomatic patients with nonvalvular AF who underwent TEE before transcatheter AF ablation (76 men; mean age 63 ± 10 years). Left atrial (LA) abnormalities such as LA thrombus, spontaneous echo contrast, or abnormal LA appendage emptying velocity (<20 cm/s) and complex plaques in the aortic arch defined as large plaques ≥4 mm thickness, ulcerated plaques, or mobile plaques were evaluated by TEE. All patients were screened for SBI by brain MRI. Of 103 patients, 31 (30%) showed SBI on brain MRI. Most lesions were multiple (61%) and small (<15 mm) in diameter (84%). Patients with SBI had a higher prevalence of LA abnormalities (45% vs 14%; P < .001) and complex arch plaques (45% vs 7%; P < .001) compared with those without SBI. In a multivariate logistic regression analysis including age and CHADS2 score ≥2, LA abnormalities (odds ratio 4.13; 95% CI 1.34-12.72; P = .014) and complex arch plaques (odds ratio 4.82; 95% CI 1.23-18.92; P = .024) were independent predictors of SBI. Left atrial abnormalities and complex arch plaques detected by TEE were closely associated with the presence of SBI on brain MRI, suggesting that microembolization of small thrombi derived from the fibrillating LA or advanced aortic atherosclerotic lesions may be important causes of SBI in patients with nonvalvular AF.

Increased Silent Brain Infarction Accompanied With High Prevalence of Diabetes and Dyslipidemia in Psychiatric Inpatients: A Cross-Sectional Study.

Patients with schizophrenia have increased risk of atherosclerotic diseases. It is already known that lifestyle-related disorders and the use of antipsychotics are closely related with the progression of atherosclerosis in psychiatric patients. Stroke as well as coronary heart disease play an important role in the cause of death in Asia and Japan. Thus, we studied the prevalence of cerebrovascular disease in psychiatric inpatients in Japan using brain magnetic resonance imaging (MRI). This cross-sectional study was performed from January 2012 to December 2013. Study participants were 152 hospitalized patients (61 men and 91 women) in the Department of Psychiatry at Kohnodai Hospital, National Center for Global Health and Medicine, Ichikawa City, Japan. Mean ages were 50.0 and 57.1 years old for men and women, respectively. The diagnoses (DSM-IV-TR criteria) of participants were schizophrenia (69.1%), mood disorder (18.4%), and other mental disorders (12.5%). We checked physical status, metabolic status of glucose and lipid levels, and brain MRI within 1 week of admission. The study group showed a significantly high prevalence of diabetes and low high-density lipoprotein (HDL) cholesterolemia in both sexes (n = 61 in men, n = 91 in women, P < .05). In the study group, serum fasting plasma glucose and hemoglobin A1c levels were significantly high (n = 152, P < .05), but serum HDL cholesterol and total cholesterol were significantly low in both sexes (n = 61 in men, n = 90 in women, P < .05), and triglycerides were low in men (n = 61, P < .05). Silent brain infarction was recognized at a higher rate (n = 98, P < .05) compared with healthy controls. Participants in this study had an increased ratio of silent brain infarction compared with Japanese healthy controls, accompanied with higher ratios of diabetes and low HDL cholesterol.

Silent brain infarcts in two patients with zeta chain-associated protein 70 kDa (ZAP70) deficiency

Zeta-chain associated protein 70kDa deficiency (ZAP70) is a form of severe combined immunodeficiency (SCID). It is caused by defects in the signaling pathways associated with T-lymphocyte activation. ZAP70 deficiency is characterized by a marked reduction in peripheral CD8+ T-cells. In this report, we described two patients with ZAP70 deficiency who presented with recurrent infections, lung tuberculosis (TBC), congenital nephrotic syndrome (CNS), and silent brain infarcts (SBIs) as a common feature. The first patient initially presented with recurrent infections and TBC as in a classic SCID patient. At the age of 4, he was interned with febrile seizure. Cranial magnetic resonance imaging (MRI) showed SBIs. The second patient, an 8-month-old boy, presented with congenital nephrotic syndrome caused by cytomegalovirus (CMV) and he had also SBIs.

Abstract MP73: Leisure Time Physical Activity and Cognitive Decline in the Northern Manhattan Study

Background: Leisure time physical activity (LTPA) has been associated with a lower risk of dementia, but whether the effects are specific to particular cognitive abilities or improvement in functional status remains unclear. We examined LTPA in relation to domain-specific neurocognitive (NC) performance and change over time in a diverse community sample. Methods: Data on LTPA was collected during enrollment (1993-2001) into the Northern Manhattan Study (NOMAS), a prospective cohort study of risk factors for stroke and cognitive decline, using a validated in-person questionnaire, and two waves of NC assessments were done on a subcohort of participants undergoing brain MRI an mean of six and 12 years later (NC1: 2003-2008; NC2: 2008-2014). Baseline LTPA was defined in two manners: (1) maximum intensity of all activities performed categorized as moderate-heavy, light, and none; (2) total summarized as a continuous variable with the metabolic equivalent (MET) score, a composite of total reported intensity and time. Factor analysis-derived construct-relevant cognitive domains, including memory (MEM), executive function (EXEC), processing speed (PS), and language ability (LA), were computed by averaging z-transformed NC test scores. We used multivariable linear regression to examine LTPA in relation to baseline domain-specific NC performance, and change in performance over time, adjusting for socio-demographics, vascular risk factors, and MRI markers of cerebrovascular injury (white matter hyperintensity volume and total cerebral volume, both adjusted for total intracranial volume, and silent brain infarcts). Results: There were 1236 participants (mean age=64 years, 61% women, 67% Latino, 18% black, 15% white) with LTPA and NC data, and 879 with a second NC assessment. Moderate-to-heavy activity was associated with higher baseline LA (p &lt;0.05) and PS (p &lt;0.05), and with a protective effect on change of MEM (p &lt;0.05) and PS (p &lt;0.05); these effects were not attenuated after adjustment for MRI variables. Total MET-score was not associated with baseline NC domain performance. However, participants with greater MET-scores had significantly less decline in processing speed adjusting for age and education. Inclusion of vascular risk factors and MRI markers each attenuated these associations though they remained statistically significant. Conclusions: Leisure time physical activity is independently protective against a decline in processing speed and memory, and was partly mediated by MRI markers. Leisure-time physical activity may protect against dementia through preventing cerebrovascular correlates of brain injury.

Stroke subtypes and factors associated with ischemic stroke in Kinshasa, Central Africa.

Ischemic stroke causes death and disability worldwide. Better understanding and controlling factors associated will improve the prevention of the disease. This study reviews records of patients with ischemic stroke in Central Africa. Patients of Bantu ethnicity with clinical diagnosis of stroke and lesion on computed tomography scan from January 2011 to December 2012 were selected. Computed tomographic subtypes of ischemic stroke and factors associated were considered with tropical seasonal variation. Of the 303 first-ever stroke patients (average age 53 years old, range 3- 84 years old; 62% male) were included in the study. The prevalence of computed tomography stroke subtypes was: lacunar infarct (63%) and non lacunar infarct lesion (37%). Silent brain infarct was seen in 9 % of patients. Prevalence of factors associated with ischemic stroke was: age≥60 years old (55%); male gender (63%), chronic and uncontrolled hypertension (54%) and type 2 Diabetes mellitus (11%). A seasonal high prevalence was observed in warmer season (p < 0.05). This study shows a high prevalence of lacunar infarct than non lacunar in Bantu of Central Africa.

Association of Mild Kidney Dysfunction with Silent Brain Lesions in Neurologically Normal Subjects

Background: Chronic kidney disease (CKD) has been closely associated with stroke. Although a large number of studies reported the relationship between CKD and different types of asymptomatic brain lesions, few comprehensive analyses have been performed for all types of silent brain lesions. Methods: We performed a cross-sectional study involving 1,937 neurologically normal subjects (mean age 59.4 years). Mild CKD was defined as an estimated glomerular filtration rate between 30 and 60 ml/min/1.73 m² or positive proteinuria. Results: The prevalence of mild CKD was 8.7%. Univariate analysis revealed an association between CKD and all silent brain lesions, including silent brain infarction, periventricular hyperintensity, subcortical white matter lesion, and microbleeds, in addition to hypertension and diabetes mellitus after adjusting for age and sex. In binary logistic regression analysis, the presence of CKD was a significant risk factor for all types of silent brain lesions, independent of other risk factors. Conclusions: These results suggest that mild CKD is independently associated with all types of silent brain lesions, even in neurologically normal subjects.