Asymptomatic Lacunar Infarcts Research Articles

Initial clinical experience with N-hexyl cyanoacrylate for neuroendovascular embolization.

To report our initial clinical experience with N-hexyl cyanoacrylate (NHCA), a novel liquid agent for neurovascular embolization. Four paragangliomas were treated with percutaneous embolization using NHCA as the sole embolic material. In one dural arteriovenous fistula (dAVF), NHCA was used in combination with other embolic materials. Procedural specifics, complications and angiographic results were retrospectively evaluated. Total or subtotal devascularization was obtained in 3 of the 4 paragangliomas. In the largest tumor, only partial devascularization could be achieved. The dAVF was completely occluded. Catheter entrapment did not occur. After dAVF treatment, the patient had an asymptomatic lacunar infarction, while there was no procedural morbidity related to paraganglioma treatment. In this series, neurovascular embolization with NHCA was feasible and effective. It may be particularly beneficial for small and tortuous vessels that require low-profile catheterization and a slow and controlled polymerization. Further studies are necessary to prove the benefits of NHCA over established embolic agents.

Asymptomatic cerebral findings on 3-Tesla MRI in patients with severe carotid artery stenoses

Background and purposeSmall vessel diseases (SVDs) are often asymptomatic. However, SVDs significantly influence the prognosis in patients with large vessel diseases (LVDs). We investigated asymptomatic cerebral findings on 3-Tesla MRI in patients with severe carotid artery (CA) stenoses, compared to peoples without a past history of neurological disorders, including strokes. MethodsWe retrospectively analyzed the prevalences of various asymptomatic cerebral findings which were intracerebral hemorrhages (ICHs), cortical superficial siderosis, ventricular dilatation (Evans’ index) and SVDs including cerebral microbleeds (CMBs), lacunar infarctions (LIs), deep white matter hyperintensities (WMHs), periventricular hyperintensities (PVHs). The prevalence of each finding was compared using multivariate logistic regression models with adjustment for stroke risk factors. ResultsWe evaluated the findings in 54 patients with severe CA stenosis treated by stenting (CA stenosis group) and 200 adults with health screening tests of the brain and no past history of neurological disorders (control group). Multivariate analyses adjusted for age ≥ 65 years old, female gender, hypertension, hyperlipidemia, diabetes mellitus, alcohol consumption, and smoking index revealed that the prevalences of severe PVHs, severe deep WMHs, asymptomatic deep ICHs, and asymptomatic LIs were significantly higher in the CA stenosis group than the control group. However, there were no significant differences in the prevalences of CMBs, or the remaining asymptomatic findings described above. ConclusionsWith pathological differences between SVD and LVD, asymptomatic SVDs except CMBs and deep ICHs often co-exists severe CA stenosis as a presentative LVD.

Plasma osteoprotegerin levels are associated with the presence and burden of cerebral small vessel disease in patients with acute ischemic stroke

Background and purposeOsteoprotegerin (OPG) is a component of the tumor necrosis factor receptor superfamily. Several studies have shown a relationship between OPG and cardiovascular diseases. We hypothesized that there is a relationship between plasma OPG levels and cerebral small vessel disease (SVD). MethodsPatients diagnosed with their first cerebral ischemic infarction between April 2014 and March 2017 were enrolled. All the enrolled patients were evaluated through the hospital stroke protocol, including routine blood tests, brain imaging, and measuring the plasma OPG levels. The presence and burden of cerebral SVD [cerebral microbleeds (CMBs), asymptomatic lacunar infarction (ALI), high-grade perivascular space (HPVS), high-grade white matter hyperintensity (HWMH)], and total SVD score were assessed through brain magnetic resonance imaging. ResultsOf the 270 patients included in our study, 158 (58.5%) were men. The mean age of the patients was 63.8 ± 11.6 years. In multivariable analysis, plasma OPG levels were positively associated with the presence and burden of each cerebral SVD. The odds ratios (OR) of CMBs, ALI, HPVS, and HWMH for the association of OPG per standard deviation (SD) increase were 1.58 [95% confidence interval (CI), 1.09–2.27], 1.40 (95% CI, 1.04–1.88), 1.88 (95% CI, 1.27–2.78), and 1.47 (95% CI, 1.04–2.08), respectively. Plasma OPG levels were positively correlated with total SVD score (beta = 0.211, standard error = 0.061, p-value = 0.009, R2 = 0.275). ConclusionsPlasma OPG levels correlate with the presence and burden of cerebral SVD in patients with acute ischemic stroke.

Risk factors for cerebral infarction in Takayasu arteritis: a single-centre case-control study.

We aimed to investigate the clinical features of Takayasu arteritis with cerebral infarction, and the risk factors for cerebral infarction. The study analysed 122 consecutive patients with Takayasu arteritis retrospectively. The clinical characteristics of Takayasu arteritis patients with and without cerebral infarction were compared. Binary logistic regression analysis was performed to determine risk factors for cerebral infarction in Takayasu arteritis patients. Cerebral infarction was present in 42 (34.4%) of 122 patients with Takayasu arteritis. There were 33 patients with ischaemic stroke and 11 with asymptomatic lacunar infarction, including two patients with both types of infarction. The cerebral infarction group had a significantly higher proportion of males, higher prevalence of blurred vision, and higher Indian Takayasu Clinical Activity Score (ITAS) 2010 than the non-cerebral infarction group. Binary logistic regression analysis indicated that hyperlipidaemia [odds ratio (OR) 5.549, P=0.021], ITAS 2010 (OR 1.123, P= 0.023), number of involved arteries (OR 1.307, P=0.018), and middle cerebral artery (MCA) involvement (OR 4.013, P=0.029) were significantly associated with cerebral infarction in patients with Takayasu arteritis. Receiver operating characteristic curves indicated fair performance of the ITAS 2010 (>6) and number of involved arteries (> 7) for distinguishing Takayasu arteritis patients at risk of cerebral infarction from those without such risk. Hyperlipidaemia, higher ITAS 2010, larger number of involved arteries, and MCA involvement are independent risk factors for cerebral infarction in Takayasu arteritis patients.

Impact of Circadian Blood Pressure Pattern on Silent Cerebral Small Vessel Disease: A Systematic Review and Meta-Analysis.

BackgroundAbnormal circadian blood pressure (BP) variations during sleep, specifically the non‐dipping (<10% fall in nocturnal BP) and reverse‐dipping patterns (rise in nocturnal BP), have been associated with an increased risk of cardiovascular events and target organ damage. However, the relationship between abnormal sleep BP variations and cerebral small vessel disease markers is poorly established. This study aims to assess the association between non‐dipping and reverse‐dipping BP patterns with markers of silent cerebral small vessel disease.Methods and Results MEDLINE, Embase, and Cochrane Databases were searched from inception through November 2019. Studies that reported the odds ratios (ORs) for cerebral small vessel disease markers in patients with non‐dipping or reverse‐dipping BP patterns were included. Effect estimates from the individual studies were extracted and combined using the random‐effect, generic inverse variance method of DerSimonian and Laird. Twelve observational studies composed of 3497 patients were included in this analysis. The reverse‐dipping compared with normal dipping BP pattern was associated with a higher prevalence of white matter hyperintensity with a pooled adjusted OR of 2.00 (95% CI, 1.13–2.37; I2=36%). Non‐dipping BP pattern compared with normal dipping BP pattern was associated with higher prevalence of white matter hyperintensity and asymptomatic lacunar infarction, with pooled ORs of 1.38 (95% CI, 0.95–2.02; I2=52%) and 2.33 (95% CI, 1.30–4.18; I2=73%), respectively. Limiting to only studies with confounder‐adjusted analysis resulted in a pooled OR of 1.38 (95% CI, 0.95–2.02; I2=52%) for white matter hyperintensity and 1.44 (95% CI, 0.97–2.13; I2=0%) for asymptomatic lacunar infarction.ConclusionsThe non‐dipping and reverse‐dipping BP patterns are associated with neuroimaging cerebral small vessel disease markers.

Impact of obstructive sleep apnea on silent cerebral small vessel disease: a systematic review and meta-analysis

BackgroundCerebral small vessel disease (CSVD) is a well-known cause of vascular dementia, a leading medical morbidity in the aging population. Obstructive sleep apnea (OSA) has been validated as a cardiovascular risk factor. However, the relationship between these two clinical syndromes is not well established. We aimed to assess the association between OSA and CSVD. MethodsDatabases were searched from inception through May 2019. Studies that reported incidence or odd ratios of CSVD in patients with OSA were included. Effect estimates from the individual studies were extracted and combined using random-effect, generic inverse variance method of DerSimonian and Laird. ResultsA total of 14 observational studies comprising of 4335 patients were included into the analysis. Compared to patients without OSA, patients with OSA were significantly associated with CSVD magnetic resonance imaging (MRI) findings of white matter hyperintensity (WMH) and asymptomatic lacunar infarction (ALI) with a pooled OR of 2.31 (95% confidence interval [CI], 1.46–3.66, I2 = 79%) and 1.78 (95% CI, 1.06–3.01, I2 = 41%), respectively. However, there was no significant association between OSA and findings of cerebral microbleeds (CMBs), with a pooled odds ratio (OR) of 2.15 (95% CI, 0.64–7.29, I2 = 55%). ConclusionsOur study demonstrated the association between OSA and CSVD MRI findings of white matter hyperintensity (WMH) and asymptomatic lacunar infarction (ALI) when compared to patients without OSA. The absence of an association of CMBs findings with OSA could be due either by a lower sensitivity of neuroimaging techniques utilized to detect CMBs or a potentially different pathogenesis of CMBs.

Association of Ultrasonography and MRI Findings with Stroke Recurrence: Differences Between Patients with Past Histories of Atherothrombotic Versus Lacunar Infarctions

Objective: This study investigated the association of MRI and ultrasonography findings with stroke recurrence in patients with past histories of atherothrombotic infarctions (ATIs) or lacunar infarctions (LIs). Methods: We prospectively analyzed the incidence of stroke recurrence. Deep and lobar cerebral microbleeds (MBs), asymptomatic lacunae, asymptomatic intracerebral hemorrhages (ICHs), severe white matter lesions (WML), and intima-media thickness (IMT) were investigated on enrollment. Stroke recurrence rates were compared by using the log-rank test. The odds ratios for recurrent strokes were derived using multivariate logistic regression models, adjusted for risk factors. Results: We evaluated the stroke recurrence rate in 362 ATI patients and 309 LI patients. The log-rank test and multivariate analyses revealed that the incidence of recurrent stroke was significantly higher in ATI patients with mean IMT greater than or equal to 1.1 mm, asymptomatic ICHs, or lobar MBs than in those without. The incidence was significantly higher in LI patients with asymptomatic ICHs, asymptomatic LIs, and severe WMLs than in those without. In ATI patients, those with strictly lobar MBs or mixed MBs (deep and lobar MBs) had significantly higher recurrence rates than those without MB. In LI patients, those with strictly deep MBs or mixed MBs had higher recurrence rates than those without MB, and the incidences of those with mixed MBs was larger than those with strictly deep MBs. Conclusions: There were differences between ATI and LI patients in terms of the association of MRI and ultrasonography findings, in particularly strictly lobar or deep MBs, with the incidence of stroke recurrence.

Plasma Klotho concentration is associated with the presence, burden and progression of cerebral small vessel disease in patients with acute ischaemic stroke.

Klotho is a soluble or membrane-bound anti-aging protein, whose protective actions are important for a prudential function of many organs. Because Klotho and cerebral small vessel disease (SVD) are associated with ageing process and endothelial dysfunction, it is possible that Klotho has an association with cerebral SVD. We aimed to investigate the association of plasma Klotho concentration with the presence, burden and progression of cerebral SVD. We prospectively enrolled 262 patients with first-ever acute cerebral infarction, performed brain MRI and collected their blood samples within 24 hours of admission. An enzyme-linked immunosorbent assay was used for evaluating plasma Klotho concentration. We estimated the total SVD score of each patient after determining the presence and burden of high-grade white matter hyperintensities (HWMHs), cerebral microbleeds (CMBs), high-grade perivascular spaces (HPVSs) and asymptomatic lacunar infarctions (ALIs). Univariate and multivariate analyses were conducted to investigate association of Klotho with cerebral SVD and the total SVD score. Of the 262 patients, 152 (58.0%) were men. The mean age of these patients was 64.7 years. The mean ± standard deviation of plasma Klotho concentration was 329.8 ± 194.1 pg/mL. In multivariate analysis, plasma Klotho concentration was negatively associated with the presence of HWMHs [Odds ratio (OR): 0.13, p = 0.047], HPVSs (OR: 0.22, p = 0.024) and ALIs (OR: 0.53, p = 0.021) but not associated with the presence of CMBs (OR: 0.39, p = 0.404). Plasma Klotho concentration was also negatively related to the total SVD score (unstandardized coefficients beta: −0.895, standard error = 0.317, p = 0.005, R2 = 0.239). Furthermore, plasma Klotho concentration was negatively related to the presence (OR: 0.75, 95% CI: 0.59–0.96, p = 0.025) and severity of cerebral SVD progression (OR: 0.72, 95% CI: 0.56–0.92, p = 0.009). In conclusion, plasma Klotho concentration was negatively associated with the presence, burden and progression of cerebral SVD.

Interarm Blood Pressure Difference has Various Associations with the Presence and Burden of Cerebral Small-Vessel Diseases in Noncardioembolic Stroke Patients.

Background and PurposeAn interarm blood pressure difference (IABD) is independently related to the occurrence of cardiovascular disease and mortality. Cerebral small-vessel diseases (SVDs) are important risk factors for stroke, cognitive dysfunction, and mortality. We aimed to determine whether IABD is related to cerebral SVDs.MethodsThis study included 1,205 consecutive noncardioembolic ischemic stroke patients as confirmed by brain MRI and simultaneously measured the bilateral brachial blood pressures. We investigated cerebral SVDs based on high-grade white-matter hyperintensities (HWHs), presence of cerebral microbleeds (CMBs), high-grade perivascular spaces (HPVSs), and asymptomatic lacunar infarctions (ALIs) on brain MRI.ResultsIn multivariate logistic regression, an interarm systolic blood pressure difference (IASBD) ≥10 mm Hg was independently related to the existence of HWHs [odds ratio (OR)=1.94, 95% CI=1.32–2.84, p=0.011] and had a tendency to be associated with the presence of HPVSs (OR=1.45, 95% CI=0.49–2.23, p=0.089) and ALIs (OR=1.42, 95% CI=0.96–2.11, p=0.052), but not with the presence of CMBs (OR=1.09, 95% CI=0.73–1.61, p=0.634). In multivariate linear regression adjusted for age, sex, and variables with p<0.1 in the univariate analysis, IASBD ≥10 mm Hg and interarm diastolic blood pressure difference ≥10 mm Hg were significantly correlated with an increased total burden of SVDs (β=0.080 and p=0.006, and β=0.065 and p=0.023, respectively).ConclusionsThis study found that IABD ≥10 mm Hg was associated with the presence and increased burden of cerebral SVDs in noncardioembolic stroke patients. This suggests that IABD ≥10 mm Hg could be a useful indicator of the presence and burden of cerebral SVDs in stroke patients.

Association between periodic limb movements during sleep and cerebral small vessel disease

ObjectivePeriodic limb movements (PLMs) can increase the risk of cardiovascular disease and mortality. Small vessel disease (SVD) has been considered a precursor to symptomatic stroke. We aimed to investigate the association between PLMs and cerebral SVD. MethodsWe enrolled participants who visited our clinic for the evaluation of sleep disturbance and underwent overnight polysomnography and brain magnetic resonance imaging. The processing steps included rating and analyzing white matter hyperintensities (WMHs), cerebral microbleeds (CMBs), asymptomatic lacunar infarctions (ALIs), perivascular spaces (PVSs), and calculating the total SVD score. Logistic regression and correlation analyses were used to examine the association between PLMs during sleep (PLMS) and SVD. ResultsA total of 31 (19 men and 12 women) patients with PLMS index ≥ 15/h were enrolled. The mean age was 61.7 years and the median PLMS index was 46.5/h. A total of 29 controls (16 men and 13 women) with PLMS index < 5/h were also included. PLMS index was positively associated with an increase in WMHs, ALIs, and PVSs (odds ratio [OR] = 1.022, 95% confidence interval [CI] = 1.003–1.040, p = 0.008; OR = 1.024, 95% CI = 1.006–1.043, p = 0.010; OR = 1.029, 95% CI = 1.010–1.049, p = 0.003, respectively). Correlation analyses revealed that total SVD score was significantly correlated with PLMS index (r = 0.504, p < 0.001). ConclusionsAn elevated PLMS index was associated with an increase in WMHs, ALIs, PVSs, and total SVD burden. Our study suggests that PLMS is a marker for SVD, which carries a potential risk for progression to overt stroke or cognitive impairment.

High dietary glycemic load was associated with the presence and burden of cerebral small vessel diseases in acute ischemic stroke patients

Cerebral small vessel diseases (SVDs) are closely associated with stroke. Elevated postprandial blood glucose is also an important risk factor for stroke. Dietary glycemic load (GL) and glycemic index (GI) are frequently used as markers of postprandial blood glucose response used as an estimator of the overall glycemic effect of the diet. We hypothesized that high dietary GL or GI will be associated with presence of cerebral SVDs in patients with acute ischemic stroke. We prospectively included 263 patients who had experienced first-ever symptomatic cerebral infarction within 7 days after symptom onset and who submitted a fully filled-in semi-quantitative food frequency questionnaire. The dietary GL and GI values of food were constructed through an International table based on glucose. The presence and burden of high-grade white matter hyperintensities (HWMHs), cerebral microbleeds (CMBs), high-grade perivascular spaces (HPVSs) and asymptomatic lacunar infarctions (ALIs) were investigated. Mean age of the total patient population was 65.4 ± 11.7 years. After adjusting for age, sex, and variables with P < .1 in univariate analysis, high dietary GL was independently associated with an increased risk of presence of HWMHs (odds ratio (OR) (95% confidence interval (CI)) comparing the top quartile with the bottom quartile: 3.31 (1.37-7.98); P (for trend) = .006), CMBs (OR (95% CI): 3.06 (1.06-8.85); P = .032), PVSs (OR (95% CI): 3.24 (0.75-13.90); P = .039), and ALIs (OR (95% CI): 2.44 (0.97-6.13); P = .037). In conclusion, high dietary GL was associated with the presence and burden of cerebral SVDs in patients with acute cerebral infarction.

Etiology of isolated pontine infarctions: a study based on high-resolution MRI and brain small vessel disease scores

BackgroundIn this retrospective study, we investigated the main pathogenesis of the two types of isolated pontine infarction: paramedian pontine infarcts (PPIs) and small deep pontine infarcts (SDPIs).MethodsAcute ischemic stroke patients, comprising 117 PPI patients and 40 SDPI patients, were enrolled. High-resolution magnetic resonance imaging (HR-MRI) and routine MRI sequences were performed for each patient, and clinical data were collected. The following brain small vessel disease (SVD) features of the MRI scans were each rated (0 or 1) separately: asymptomatic lacunar infarcts, white matter lesions (WMLs), deep and infratentorial cerebral microbleeds (CMBs), and enlarged perivascular spaces in the basal ganglia. The ratings were also summed in an ordinal “SVD score” (range: 0–4). The difference in the SVD score between the PPI and SDPI groups was determined. The presence and location of basilar artery (BA) atherosclerotic plaques (based on HR-MRI) in the two groups was evaluated.ResultsThere was a significant difference in the total SVD score and three of the four independent SVD features (asymptomatic lacunar infarcts, WMLs, and deep and infratentorial CMBs) between the two groups. The prevalence of BA plaques relevant to the infarcts in the PPI group was significantly higher than that in the SDPI group, whereas the prevalence of plaques irrelevant to the infarcts was similar between the two groups. The degree of BA stenosis was slightly higher in the PPI group than in the SDPI group. Diabetes mellitus was much more prevalent in the PPI group. The National Institute of Health Stroke Scale score was higher in the PPI group, which is in accordance with the larger infarct size in the PPI group.ConclusionBA atherosclerosis may be the major cause of PPI, while SVD may be the main mechanism underlying SDPI. HR-MRI combined with the total SVD score should be helpful to explore the pathogenesis underlying isolated pontine infarctions, especially in cases involving low-grade BA stenosis.

Total Cerebral Small-Vessel Disease Score is Associated with Mortality during Follow-Up after Acute Ischemic Stroke.

Background and PurposeThe recently developed total cerebral small-vessel disease (CSVD) score might appropriately reflect the total burden or severity of CSVD. We investigated whether the total CSVD score is associated with long-term outcomes during follow-up in patients with acute ischemic stroke.MethodsIn total, 1,096 consecutive patients with acute ischemic stroke who underwent brain magnetic resonance imaging were enrolled. We calculated the total CSVD score for each patient after determining the burden of cerebral microbleeds (CMBs), high-grade white-matter hyperintensities (HWHs), high-grade perivascular spaces (HPVSs), and asymptomatic lacunar infarctions (ALIs). We recorded the date and cause of death for all of the patients using data from the Korean National Statistical Office. We compared the long-term mortality rate with the total CSVD score using Cox proportional-hazards models.ResultsCMBs were found in 26.8% of the subjects (294/1,096), HWHs in 16.4% (180/1,096), HPVSs in 19.3% (211/1,096), and ALIs in 38.0% (416/1,096). After adjusting for age, sex, and variables that were significant at p<0.1 in the univariate analysis, the total CSVD score was independently associated with long-term death from all causes [hazard ratio (HR)=1.18 per point, 95% confidence interval (CI)=1.07–1.30], ischemic stroke (HR=1.20 per point, 95% CI=1.01–1.42), and hemorrhagic stroke (HR=2.05 per point, 95% CI=1.30–3.22), but not with fatal cardiovascular events (HR=1.17 per point, 95% CI=0.82–1.67).ConclusionsThe total CSVD score is a potential imaging biomarker for predicting mortality during follow-up in patients with acute ischemic stroke.

Total magnetic resonance imaging burden of cerebral small-vessel disease is associated with post-stroke depression in patients with acute lacunar stroke.

Despite extensive studies on post-stroke depression (PSD), the role of the total burden of cerebral small-vessel disease (cSVD) in its pathogenesis remains unclear. We conducted a magnetic resonance imaging (MRI)-based cohort study to investigate the relationship between total MRI burden of cSVD and PSD among patients with first-ever lacunar stroke. From June 2013 to January 2016, 374 patients were consecutively recruited. PSD was identified using the Chinese version of the Structured Clinical Interview for DSM-IV. Brain MRI presence of silent lacunar infarcts, white-matter lesions, cerebral microbleeds and enlarged perivascular spaces was summed to an ordinal score between 0 and 4. Multivariable logistic regression analysis was performed to determine the contribution of total MRI cSVD burden in the prediction of PSD. Ninety patients (24.1%) were diagnosed with PSD at 3months after stroke. Only two MRI markers of cSVD, asymptomatic lacunar infarcts and white-matter lesions, were related to PSD [odds ratio (OR), 3.167; 95% confidence interval (CI), 1.879-5.338; P=0.001 and OR, 2.284; 95% CI, 1.403-3.713; P=0.001, respectively]. Moreover, higher total MRI cSVD burden was an independent predictor for PSD (high tertile OR, 4.577; 95% CI, 2.400-8.728; P=0.001) after adjusting for individual cSVD MRI marker and other potential confounders. This study demonstrated that greater total MRI burden of cSVD may predict the presence of PSD in patients with acute lacunar stroke.

Association between Aortic Atheroma and Cerebral Small Vessel Disease in Patients with Ischemic Stroke

Background and PurposeCerebral small vessel disease (SVDs) are related with large artery atherosclerosis. However, the association between aortic atheroma (AA) and cerebral small vessel disease has rarely been reported. This study evaluated the relationship between presence and burden of AAs and those of SVDs in patients with acute ischemic stroke.MethodsWe included 737 consecutive patients who underwent transesophageal echocardiography (TEE) and brain magnetic resonance imaging (MRI) for evaluation of acute stroke. AA subtypes were classified as complex aortic plaque (CAP) and simple aortic plaque (SAP). Presence and burden of SVDs including cerebral microbleeds (CMBs), white matter hyperintensities (WMHs), perivascular spaces (PVSs), asymptomatic lacunar infarctions (ALIs), and total SVD score, were investigated.ResultsAA was found by TEE in 360 (48.8%) patients including 11.6% with CAP and 37.2% with SAP. One or more types of SVDs was found in 269 (36.4%) patients. In multivariable analysis, presence of CMBs (odds ratio [OR] 4.68), high-grade WMHs (OR 3.13), high-grade PVSs (OR 3.35), and ALIs (OR 4.24) were frequent in patients with AA than those without AA. Each 1-point increase in total SVD score increased the odds of presence of CAP (OR 1.94, 95% confidence interval (CI) 1.44-1.85) and SAP (OR 1.54, 95% CI 1.35-1.75).ConclusionsIn this study, patients with AA frequently had cerebral SVDs. Larger burden of AA was associated with advanced cerebral SVDs. Our findings give an additional information for positive relationship with systemic atherosclerosis and coexisting cerebral SVDs in acute ischemic stroke patients.

Pathogenesis and neuroimaging of cerebral large and small vessel disease in type 2 diabetes: A possible link between cerebral and retinal microvascular abnormalities.

Diabetes patients have more than double the risk of ischemic stroke compared with non‐diabetic individuals, and its neuroimaging characteristics have important clinical implications. To understand the pathophysiology of ischemic stroke in diabetes, it is important to focus not only on the stroke subtype, but also on the size and location of the occlusive vessels. Specifically, ischemic stroke in diabetes patients might be attributed to both large and small vessels, and intracranial internal carotid artery disease and small infarcts of the posterior circulation often occur. An additional feature is that asymptomatic lacunar infarctions are often seen in the basal ganglia and brain stem on brain magnetic resonance imaging. In particular, cerebral small vessel disease (SVD), including lacunar infarctions, white matter lesions and cerebral microbleeds, has been shown to be associated not only with stroke incidence, but also with the development and progression of dementia and diabetic microangiopathy. However, the pathogenesis of cerebral SVD is not fully understood. In addition, data on the association between neuroimaging findings of the cerebral SVD and diabetes are limited. Recently, the clinical importance of the link between cerebral SVD and retinal microvascular abnormalities has been a topic of considerable interest. Several clinical studies have shown that retinal microvascular abnormalities are closely related to cerebral SVD, suggesting that retinal microvascular abnormalities might be pathophysiologically linked to ischemic cerebral SVD. We review the literature relating to the pathophysiology and neuroimaging of cerebrovascular disease in diabetes, and discuss the problems based on the concept of cerebral large and small vessel disease.

Moderate-to-severe obstructive sleep apnea is associated with cerebral small vessel disease

BackgroundCerebral small vessel disease (SVD) is associated with increased risk of cerebral infarction and hemorrhage. Obstructive sleep apnea (OSA) is known to increase the risk of cerebrovascular disease. This study aimed to investigate the association between cerebral SVD and severity of OSA. MethodsA total of 170 patients were included from the patient registry at the present Sleep Center; these patients underwent both magnetic resonance imaging (MRI) of the brain and polysomnography (PSG) for suspected OSA. The presence and burden of white matter hyperintensities (WMHs), asymptomatic lacunar infarctions (ALIs), cerebral microbleeds (CMBs), and perivascular spaces (PVSs) were determined by MRI, and their relationships with the apnea–hypopnea index (AHI), as determined by PSG, were investigated. ResultsAmong the 170 patients, 25 (14.7%) had high-grade WMHs, 21 (12.4%) had ALIs, 21 (12.4%) had CMBs, and 34 (20.0%) had high-grade PVSs. In the multivariable analysis, after adjusting for factors including age, sex, and other variables for which p < 0.1 in univariable analysis (hypertension, diabetes mellitus, previous stroke, minimal SaO2 and arousal index), moderate-to-severe OSA was associated with high-grade WMHs (odds ratio [OR] 4.72; 95% confidence interval [CI] 1.14–19.47), CMBs (OR 3.47; 95% CI 0.89–15.18), or high-grade PVSs (OR 3.64; 95% CI 1.02–13.01), but not with ALIs. The total SVD score was independently associated with increased AHI (p = 0.017), particularly in patients with moderate-to-severe OSA (β [standard error] = 0.448 (0.204), p = 0.030]. ConclusionModerate-to-severe OSA is positively associated with multiple indicators of cerebral SVD, including WMHs, CMBs, and PVSs.

Modification of lipoprotein and glucose metabolism, vascular inflammatory biomarkers and neuropathy after weight loss following bariatric surgery

Modification of lipoprotein and glucose metabolism, vascular inflammatory biomarkers and neuropathy after weight loss following bariatric surgery

Low levels of plasma omega 3-polyunsaturated fatty acids are associated with cerebral small vessel diseases in acute ischemic stroke patients

Cerebral small vessel diseases (SVDs) are related to stroke or cognitive dysfunction. n-3-polyunsaturated fatty acids (PUFAs) such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) represent possible disease-modifying factors for cardiovascular disease or dementia. Our hypothesis was that a low proportion of plasma FAs would be associated with cerebral SVDs. We prospectively enrolled 220 patients with a first-episode cerebral infarction within 7days after symptom onset. The composition of plasma FAs was analyzed by gas chromatography methods. The presence and burden of cerebral microbleeds (CMBs), high-grade white matter changes (HWCs), high-grade perivascular spaces (HPVSs), and asymptomatic lacunar infarctions (ALIs) were investigated. The mean proportion (±SD) was 2.0 ± 0.7 for EPA, 8.9 ± 1.5 for DHA, and 12.0 ± 2.1 for ∑ n-3-PUFAs. In total, 46 (20.9%) patients had CMBs, 64 (29.1 %) had HWCs, 57 (25.9%) had HPVSs, and 65 (29.5%) had ALIs. In univariate analyses, CMBs, HWCs, and HPVSs were each negatively correlated with the proportion of EPA, DHA, and ∑ n-3-PUFAs. In the multivariate analysis, a lower proportion of EPA, DHA and ∑ n-3-PUFAs was associated with the presence of CMBs, HWCs and HPVS, but not ALIs. Total SVDs score was inversely correlated with the proportion of EPA, DHA and ∑ n-3-PUFAs. Overall, we found an association between low proportions of plasma n-3-PUFAs and cerebral SVDs pathologies. Further studies are needed to explore the association and potential therapeutic role of FAs in cerebral SVDs.

Chronic kidney disease and cerebral small vessel disease: a casual or causal cerebrorenal relationship?

Abstract is not required for Editorialis not required for Editorial (This page in not part of the published article.) International Journal of Case Reports and Images, Vol. 6 No. 8, August 2015. ISSN – [0976-3198] Int J Case Rep Images 2015;6(8):526–529. www.ijcasereportsandimages.com Rivera-Zambrano et al. 526 CASE REPORT OPEN ACCESS Chronic kidney disease and cerebral small vessel disease: A casual or causal cerebrorenal relationship? Marx Rivera-Zambrano, Adria Arboix, Maria-Jose Sanchez Recent studies show that individuals with progressive chronic kidney disease have a greater risk of cardiovascular events, hospitalization and death [1]. Chronic kidney disease (CKD) is prevalent in acute stroke patients with rates varying from 20–35% in ischemic stroke and from 20–46% in intracerebral hemorrhage [2, 3]. Previously, a higher four to ten times, prevalence of stroke in dialysis patients have been reported [3]. It can therefore be concluded that CKD is an established and emergent risk factor for cardiovascular disease in general and for cerebrovascular disease in particular. Chronic kidney disease is defined either by a decrease in the estimated glomerular filtration rate (eGFR) below 60 ml/min/1.73 m2 or by the presence of albuminuria as a marker of an increased glomerular permeability [4]. It represents also a poor prognosis factor in patients with acute stroke and its presence has been associated with stroke severity and poor outcomes in ischemic and hemorrhagic stroke. A study reported that patients with CKD had a 49% greater risk of neurological deterioration during hospital stay and in-hospital mortality, and higher degree of disability at discharge according to the modified Rankin scale score of 2 or more than patients without CKD [5]. Greater risk of recurrence of non-cardioembolic stroke in CKD patients has also been reported [3]. This Marx Rivera-Zambrano1, Adria Arboix2, Maria-JoseSanchez3 Affiliations: 1Internal Medicine Department, Hospital Universitari Sagrat Cor. Hospital Universitari Sagrat Cor, University of Barcelona, Barcelona, Catalonia, Spain; 2Cerebrovascular Division, Neurology Department, Hospital Universitari Sagrat Cor, University of Barcelona, Barcelona, Catalonia, Spain; 3Library Department. Hospital UniversitariSagratCor, University of Barcelona, Barcelona, Catalonia, Spain. Corresponding Author: Adria Arboix, Barcelona, Catalonia, Spain, 08029; Tel.: 34 934948940; Fax: 34 934948906; Email: aarboix@hscor.com, Received: 03 June 2015 Published: 01 August 2015 EdiTO iAlS OPEN A CE S worse neurological prognosis may be caused by the presence in these patients of proteinuria and albuminuria, and both conditions are significantly associated with high levels of inflammatory cytokines and oxidative stress, inflammation and conditions promoting coagulation, potentially causing excessive vascular damage at stroke onset. These factors are also associated with accelerated atherosclerosis and endothelial dysfunction. Albuminuria is also predictive of hemorrhagic transformation of stroke [2]. We must also point out that CKD patients have both high thromboembolic and high bleeding risks and this has implications for deciding the optimal therapeutic strategy for primary or secondary prevention in these clinical conditions. Thus, non-vitamin K antagonist oral anticoagulants (novel oral anticoagulants) seem to be safer and more effective for patients with nonvalvular atrial fibrillation than warfarin, but cannot be given to patients with advanced CKD because the activity of these drugs is greatly affected by renal function [2, 6]. Intravenous thrombolysis is not contraindicated for patients with CKD but experts have limited experience with this treatment in these patients [6]. It is worth mentioning that kidney impairment is strongly associated with cerebral small vessel diseases (SVDs), which occur as asymptomatic lacunar infarcts (Figure 1) often resulting in classical lacunar syndromes (pure motor hemiparesis, pure sensory syndrome, sensorimotor stroke, ataxic hemiparesis or dysarthriaclumsy hand) or, less frequently, in atypical lacunar syndromes [7,8]. They also result in leukoaraiosis or white matter hyperintensities, silent lacunes, prominent or enlarged perivascular spaces and cerebral microbleeds [9]. One study reported that the volume of white matter lesions increased when eGFR decreased [10], and another showed that proteinuria had strong relation with both the presence and number of microbleeds [11]. This special relationship between CKD and cerebral SVDs is still unclear and warrant further investigation but is probably due to the fact that the vasoregulation of the microvasculature of the two organs (kidney and