Scattered cerebral infarction in the corona radiata predicts worse outcomes.

OBJECTIVES: Intracranial branch atheromatous disease often results in progressive motor deficits in the lenticulostriate arteries (LSA). In some patients with LSA infarction, magnetic resonance imaging (MRI) revealed single lesions at the LSA origin from the middle cerebral artery spreading in a scattered manner toward the distal area. This study aimed to elucidate the clinical characteristics of such cases. MATERIALS AND METHODS: This was a single-center, retrospective study comprising 1,840 consecutive patients admitted to the Ina Central Hospital, Japan. Two neurologists selected patients with LSA infarctions on the basis of MRI data. Patients with a single mass of infarct lesion from the origin were classified as the single group, whereas patients with infarct lesions as a single mass at LSA origin but divided and independent as the infarct area extended distally were classified as the scattered group. We compared the clinical characteristics and outcomes in these groups. RESULTS: The single and scattered groups included 119 and 35 patients, respectively. We defined worsening as an increase of one point or more on the National Institute of Health Stroke Scale. Univariate analysis demonstrated that patients in the scattered group showed significantly more worsening after hospitalization compared with those in the single group (48.6% vs. 28.6%; p < .05). Moreover, this can easily lead to increased disease severity (p < .016). In a multivariate analysis, group (odds ratio, 2.5 [95% CI, 1.11-5.74], p < .03) was an independent predictor of symptom worsening. CONCLUSIONS: Scattered infarction in the corona radiata is an aggravating factor leading to worse outcomes.

Visualization of lenticulostriate artery by intracranial dark-blood vessel wall imaging and its relationships with lacunar infarction in basal ganglia: a retrospective study.

OBJECTIVES: There is close relationship between lenticulostriate arteries (LSAs) and lacunar infarctions (LIs) of the basal ganglia. The study aims to visualize the LSAs using high-resolution vessel wall imaging (VWI) on 3T system and explore the correlation between LSAs and LIs. METHODS: Fifty-six patients with LIs in basal ganglia, and 44 age-matched control patients were enrolled and analyzed retrospectively. The raw VWI images were reformatted into coronal slices in minimum intensity projection for further observation of LSAs. The risk factors of LIs in basal ganglia were analyzed by univariate and multivariate logistic regression. The correlation and linear regression analysis between the LSAs and LIs, ipsilateral MCA-M1 plaques were investigated. RESULTS: The total number (p < 0.01) and length (p < 0.01) of LSAs were statistically different between basal ganglias with and without LIs. The total number of LSAs and ipsilateral MCA-M1 plaques were independently related to LIs in basal ganglias. The mean length of LSAs were negatively correlated with number (r = - 0.33, p = 0.002) and volume (r = - 0.37, p = 0.001) of LIs. Age, drinking history, and mean length of LSAs were associated with LI occurrence in basal ganglia, and mean length of LSAs was correlated with larger volume of LIs. CONCLUSIONS: Number of LSA reduction and ipsilateral MCA-M1 plaques were associated with the presence of LIs in basal ganglias. Age increasing, drinking history, and shorter LSAs were correlated with the increasing of LIs. KEY POINTS: • Patients with LIs tend to have shorter LSAs. • The characteristics of LSAs and ipsilateral MCA-M1 plaques are associated with LIs in basal ganglias. • Age, drinking history, and mean length of LSAs are correlated with LI features in basal ganglias.

A deep semantic segmentation correction network for multi-model tiny lesion areas detection.

BACKGROUND: Semantic segmentation of white matter hyperintensities related to focal cerebral ischemia (FCI) and lacunar infarction (LACI) is of significant importance for the automatic screening of tiny cerebral lesions and early prevention of LACI. However, existing studies on brain magnetic resonance imaging lesion segmentation focus on large lesions with obvious features, such as glioma and acute cerebral infarction. Owing to the multi-model tiny lesion areas of FCI and LACI, reliable and precise segmentation and/or detection of these lesion areas is still a significant challenge task. METHODS: We propose a novel segmentation correction algorithm for estimating the lesion areas via segmentation and correction processes, in which we design two sub-models simultaneously: a segmentation network and a correction network. The segmentation network was first used to extract and segment diseased areas on T2 fluid-attenuated inversion recovery (FLAIR) images. Consequently, the correction network was used to classify these areas at the corresponding locations on T1 FLAIR images to distinguish between FCI and LACI. Finally, the results of the correction network were used to correct the segmentation results and achieve segmentation and recognition of the lesion areas. RESULTS: In our experiment on magnetic resonance images of 113 clinical patients, our method achieved a precision of 91.76% for detection and 92.89% for classification, indicating a powerful method to distinguish between small lesions, such as FCI and LACI. CONCLUSIONS: Overall, we developed a complete method for segmentation and detection of WMHs related to FCI and LACI. The experimental results show that it has potential clinical application potential. In the future, we will collect more clinical data and test more types of tiny lesions at the same time.

Higher Cerebral Small Vessel Disease Burden in Patients with White Matter Recent Small Subcortical Infarcts.

INTRODUCTION: Recent small subcortical infarcts (RSSI) are considered an acute manifestation of cerebral small vessel disease (CSVD). We assessed whether the topography of RSSI was related to CSVD markers on magnetic resonance imaging (MRI). MATERIAL AND METHODS: We screened the local registries of two independent stroke centers in Catalonia and selected patients with a symptomatic RSSI on MRI performed during admission. RSSI location was classified into brainstem, supratentorial subcortical structures (SSS), and centrum semiovale (CSO) regions. Clinical variables, including vascular risk factors, were collected. Radiological markers of CSVD on MRI were evaluated individually and by means of the global CSVD burden score. The associations between each RSSI location and CSVD markers were studied in uni- and multivariate logistic regression analysis. RESULTS: Among 475 patients with RSSI, 152 (32%) had an infarct in the brainstem, 227 (48%) in SSS, and 96 (20%) in CSO region. The median CSVD burden score was 2 (IQR, 1-3). After adjusting for confounding factors, a RSSI in CSO was associated with higher periventricular and deep white matter hyperintensity scores [OR 1.64 (95% CI, 1.16-2.33), and OR 1.44 (95% CI, 1.07-1.93), respectively]. Higher CSVD burden score was positively associated with CSO [OR 1.48 (95% CI, 1.22-1.81)] and inversely associated with SSS [0.85 (95% CI, 0.72-0.99)] location after adjusting for relevant confounders. CONCLUSIONS: CSO RSSI were related to a higher burden of CSVD, particularly to white matter hyperintensities, compared to other RSSI locations. The pathophysiological significance of such findings should be investigated in the future with advanced neuroimaging techniques.

Susceptibility Vessel Sign in Deep Perforating Arteries in Patients with Recent Small Subcortical Infarcts.

OBJECTIVES: Recent small subcortical infarcts (RSSI) are considered an acute manifestation of cerebral small vessel disease. Paramagnetic signals in perforating arteries supplying RSSI may be detected on T2*-relaxation derived sequences on MRI and is defined as susceptibility vessel sign (SVS). We aimed to study the prevalence of SVS in patients with RSSI, and explore whether its identification is related to cerebral small vessel disease markers. MATERIALS AND METHODS: We selected patients with RSSI identified on MRI during admission from a single-center stroke registry. The main demographic and clinical features, including vascular risk factors, were collected. Radiological features of RSSI and cerebral small vessel disease [white matter hyperintensities in deep and periventricular regions, enlarged perivascular spaces, lacunae, microbleeds, and brain atrophy] were described using validated qualitative scores. The presence of SVS was assessed on T2*gradient-echo or other susceptibility-weighted imaging. We compared the clinical and radiological features of patients with or without SVS in uni- and multivariate models. RESULTS: Out of 210 patients with an RSSI on an MRI, 35 (17%) showed SVS. The proportion of SVS+ patients was similar in different susceptibility imaging modalities (p=.64). Risk factor profiles and clinical course were similar in SVS+ and SVS- patients. SVS+ patients had a higher grade of deep white matter hyperintensities and brain atrophy, more lacunae (p=.001, p=.034, p=.022, respectively), and a similar degree of the rest of radiological variables, compared to SVS- patients. In the multivariate analysis, the grade of deep white matter hyperintensities was the only independent factor associated with SVS [OR 3.1 (95% CI, 1.5-6.4)]. CONCLUSIONS: SVS in patients with RSSI is uncommon and related to a higher grade of deep white matter hyperintensities. Pathophysiological mechanisms underlying the deposition of hemosiderin in the path of occluded perforating arteries are uncertain and might include endothelial dysfunction or embolic mechanisms.

[Current state of cerebral microangiopathy in hypertension]. / Sovremennoe sostoyanie problemy tserebral'noi mikroangiopatii pri arterial'noi gipertenzii.

Hypertension is the main cause and the most important risk factor for both acute cerebrovascular accident and chronic progressive cerebrovascular insufficiency that is accompanied by severe neurological and mental disorders even to the extent of developing dementia. They are based on hypertension-induced pathology of the intracerebral arteries and cerebral microvasculature - cerebral microangiopathy that leads to small deep (lacunar) infarcts (SDIs) and diffuse cerebral white matter diseases. This review highlights the morphology, pathogenesis, clinical and neuroimaging diagnosis of hypertensive SDIs, and their differential diagnosis with atherosclerotic SDIs in the historical aspect. It is emphasized that the lacunar state of the brain in hypertension is a predictor of massive cerebral hemorrhages. Special attention is paid to current studies of the morphology and pathogenesis of diffuse changes in white matter and to the role of blood-brain barrier impermeability in the development of progressive leukoencephalopathy.

Cerebral Small Vessel Disease in Standard Pre-operative Imaging Reports Is Independently Associated with Increased Risk of Cardiovascular Death Following Carotid Endarterectomy.

OBJECTIVE: Cerebral white matter lesions (WMLs) and lacunar infarcts are surrogates of cerebral small vessel disease (SVD). WML severity as determined by trained radiologists predicts post-operative stroke or death in patients undergoing carotid endarterectomy (CEA). It is unknown whether routine pre-operative brain imaging reports as part of standard clinical practice also predict short and long term risk of stroke and death after CEA. METHODS: Consecutive patients from the Athero-Express biobank study that underwent CEA for symptomatic high degree stenosis between March 2002 and November 2014 were included. Pre-operative brain imaging (computed tomography [CT] or magnetic resonance imaging [MRI]) reports were reviewed for reporting of SVD, defined as WMLs or any lacunar infarcts. The primary outcome was defined as any stroke or any cardiovascular death over three year follow up. The secondary outcome was defined as the 30 day peri-operative risk of stroke or cardiovascular death. RESULTS: A total of 1038 patients were included (34% women), of whom 659 (63.5%) had CT images and 379 (36.5%) MRI images available. Of all patients, 697 (67%) had SVD reported by radiologists. Patients with SVD had a higher three year risk of cardiovascular death than those without (6.5% vs. 2.1%, adjusted HR 2.52 [95% CI 1.12-5.67]; p = .026) but no association was observed for the three year risk of stroke (9.0% vs. 6.7%, for patients with SVD vs. those without, adjusted HR 1.24 [95% CI 0.76-2.02]; p = .395). No differences in 30 day peri-operative risk were observed for stroke (4.4% vs. 2.9%, for patients with vs. those without SVD; adjusted HR 1.49 [95% CI 0.73-3.05]; p = .28), and for the combined stroke/cardiovascular death risk (4.4% vs. 3.5%, adjusted HR 1.20 [95% CI 0.61-2.35]; p = .59). CONCLUSION: Presence of SVD in pre-operative brain imaging reports can serve as a predictor for the three year risk of cardiovascular death in symptomatic patients undergoing CEA but does not predict peri-operative or long term risk of stroke.

Magnetic resonance imaging and risk factors for progression of lacunar infarct lesions in Chinese patients.

PURPOSE: The proportion of acute symptomatic lacunar infarction lesions that undergo cavitation and the factors influencing cavity formation are yet unclear, particularly in the Chinese population. Hence, we investigated changes in the diameter of acute lacunar infarction lesions and identified the risk factors for the progression of these lesions. METHODS: A total of 160 patients (mean age 66 years) with acute symptomatic lacunar infarction lesions underwent two magnetic resonance imaging (MRI) examinations: diffusion-weighted imaging (DWI) at onset (lesion diameter < 20 mm) and T2-weighted imaging/fluid-attenuated inversion recovery sequences at follow-up (median follow-up time 389 days). Lacunar infarction lesion progression was categorized as complete cavitation (lacune), partial cavitation, white matter lesion (WML), or disappearance of the lesion. The risk factors for cavity formation were evaluated. RESULTS: Upon follow-up MRI, lesions had changed to lacunes in 20 (12.5%) patients, partial cavitation in 23 (14.4%), WMLs in 97 (60.6%), and had disappeared in 20 (12.5%). Lacune formation was related to hypertension (P = 0.026); cavity (lacune and partial cavitation) formation was related to diabetes (P = 0.009) and diameter change (P = 0.015). CONCLUSIONS: Approximately a quarter of the acute symptomatic lacunar infarction lesions observed with follow-up MRI were cavitated. Hypertension was negatively associated with lacune formation; diabetes and diameter change were negatively associated with cavity formation.

Cavitation of symptomatic acute single small subcortical infarctions.

BACKGROUND AND PURPOSE: To investigate cavitation of symptomatic acute single small subcortical infarctions (SSSI). METHODS: Acute SSSI were diagnosed with magnetic resonance (MR) diffusion-weighted imaging (DWI) combined with apparent diffusion coefficient (ADC) sequence on follow-up MR imaging. Cavitation of the acute SSSI was comprehensively viewed on FLAIR, T2-, and T1-weighted sequences. RESULTS: We enrolled 123 patients with acute SSSI. The follow-up median interval was 303 (125-390) days. The lesions of SSSI evolved into cavitation in 93 patients (75.6%), evolved into WMHs in nine patients (7.3%), and were no visible in 21 patients (17.1%). Cavitation was independently associated with larger infarct diameter on baseline DWI [odds ratio (OR), 1.250, 95% CI (1.078-1.451), P = 0.003], higher score of baseline old lacunar infarct [OR 3.44, 95% CI (1.49-7.91), P = 0.004], and lower rate of dyslipidemia [OR 0.30, 95% CI (0.10-0.76), P = 0.013]. CONCLUSION: Cavitation occurred more in the setting of small vessel diseased brain and less in the SSSI of possible atherosclerotic etiology. This suggested that the etiology of infarct was associated with cavitation after acute SSSI.

Periodontitis as a risk indicator and predictor of poor outcome for lacunar infarct.

AIM: To investigate the association between periodontitis (PD) and lacunar infarct (LI) as well as to analyse whether PD could be a predictor of poor functional prognosis in patients with LI. MATERIAL AND METHODS: Full-mouth periodontal examination was done in 120 cases (patients with LI) and 157 healthy controls. Demographic, clinical, medical and neurological information were collected from all of them. In addition, a measure of periodontal inflammation and disease activity, namely the periodontal inflamed surface area (PISA), was also calculated for each patient. Poor functional outcome was considered as a modified Rankin Scale >2 at 3 months. RESULTS: PD was independently associated with the presence of LI (OR = 3.3, p < 0.001). Poor outcome was observed in 31 patients with LI (25.8%), of which 90.3% had PD. A PISA value ≥727 mm2 was an independent predictor of poor prognosis, after adjusting for clinical confounders (OR = 6.5, p = 0.001). CONCLUSIONS: PD and LI were associated. Active moderate to severe PD predicted poor prognosis in patients with LI. Further evidence is warranted to confirm our results and investigate potential mechanisms behind this association.

Localized atrophy of the pontine base as a sequela of prolonged ischemia: Report of an autopsy case.

An 80-year-old man with a history of diabetes mellitus and hypertension died of a progressive neurological disorder characterized by truncal ataxia, extraocular movement disturbance, and muscular rigidity. Neuroradiological examination showed progressive atrophy restricted to the pontine base. Autopsy revealed localized atrophy of the pontine base, in which both neurons and nerve fibers were lost, especially in the central region. Medium-sized and small arteries in the parenchyma of the pontine base showed marked fibro-hyalinous thickening of the walls with luminal stenosis, but no distinct tissue defect as seen in lacunar infarct was observed. Perivascular lymphocytic infiltration was mostly absent, and reactive astrocytic proliferation was weak. The pontine tegmentum, midbrain, and medulla oblongata were well preserved. Localized atrophy of the pontine base is a rare pathological condition, and its pathogenesis in the present case can be best explained by a prolonged ischemic state (hypoperfusion) due to marked sclerotic changes of perforating arteries. It is unique that the lesions were restricted to the pontine base and the formation of lacunas was not observed. Localized metabolic derangement resembling that seen in central pontine myelinolysis might have also contributed to the pathogenesis of this peculiar localized atrophy.

Non-obese fatty liver disease is associated with lacunar infarct.

BACKGROUND/AIMS: Lacunar infarct, a small subcortical ischaemic lesion, is a known risk factor for future cognitive impairment, dementia and stroke. We evaluated the relationship between fatty liver disease (FLD) and lacunar infarct in a healthy general population. METHODS: Subjects who underwent brain magnetic resonance imaging (MRI) and abdominal ultrasonography (US) during health check-ups from 2007 to 2009 were included. FLD was diagnosed by US. Subjects with a history of cerebrovascular disease, radiological findings consistent with cerebrovascular stenosis or cerebral small vessel disease were excluded. RESULTS: Of the 1277 subjects, 54 (4.2%) exhibited lacunar infarct, and 514 (40.3%) had FLD. Subjects with lacunar infarct had a higher prevalence of FLD (59.3% vs 39.4%, P = .004). There was significant interaction between obesity (BMI < 25 kg/m2 vs ≥ 25 kg/m2 ) and FLD for lacunar infarct (P for interaction = .024). Subgroup analysis revealed that non-obese FLD was more common in the subjects with lacunar infarct than those without (51.7% vs 23.5%, P = .001). However, there was no significant difference in the obese FLD prevalence between these 2 groups. In multivariate models adjusted by age, sex, smoking, alcohol, hypertension and diabetes, FLD was significantly associated with lacunar infarct (odds ratio [OR] 1.97; 95% confidence interval [CI] 1.08-3.58; P = .027). Non-obese FLD was associated with lacunar infarct (OR 3.58; 95% CI 1.63-7.89; P = .002); however, this association remained insignificant in obese FLD. Instead, ageing and hypertension were independent risk factors for lacunar infarct in the obese population. CONCLUSIONS: FLD is significantly associated with lacunar infarct, independent of traditional risk factors. This association was prominent in the non-obese population.

Chronic Infarcts Predict Poor Clinical Outcome in Mechanical Thrombectomy of Sexagenarian and Older Patients.

BACKGROUND: The impact of lacunar and cortical chronic ischemic lesions (CILs) on the clinical outcome of mechanical thrombectomy (MT) has been little studied. Clinical trials suggest that older patients benefit from MT. We investigated the effect of CILs on the clinical outcome of sexagenarian and older patients with acute middle cerebral artery (MCA) or distal internal carotid artery (ICA) stroke who received MT to treat large-vessel occlusion (LVO). METHODS: We prospectively collected the clinical and imaging data of 130 consecutive MT patients of which 68 met the inclusion criteria. We limited the analysis to sexagenarian and older subjects and occlusions no distal than the M2 segment. Baseline clinical, procedural and imaging variables, technical outcome, 24-hour imaging outcome, and the clinical outcome were recorded. Differences between patients with and without CILs were studied with appropriate statistical tests and binary logistic regression analysis. RESULTS: Twenty-one patients (31%) had at least 1 CIL. Thirty-eight percent of patients with CIL(s) compared with 62% without (P = .06) experienced good clinical outcome (3-month modified Rankin Scale ≤ 2). A similar nonsignificant trend was seen when lacunar lesions, lesion multiplicity, and chronic white matter lesions were examined separately. Absence of CIL increased the odds of good clinical outcome 3.7-fold (95% confidence interval 1.0-10.7, P = .05) in logistic regression modeling. CONCLUSIONS: Chronic cortical and lacunar infarcts in admission imaging are associated with poor clinical outcome in sexagenarian and older patients treated with MT for LVO of the MCA or distal ICA.

Linear sign in cystic brain lesions ≥5 mm: A suggestive feature of perivascular space.

OBJECTIVE: To determine the prevalence of a linear sign within enlarged perivascular space (EPVS) and chronic lacunar infarction (CLI) ≥ 5 mm on T2-weighted imaging (T2WI) and time-of-flight (TOF) magnetic resonance angiography (MRA), and to evaluate the diagnostic value of the linear signs for EPVS over CLI. METHODS: This study included 101 patients with cystic lesions ≥ 5 mm on brain MRI including TOF MRA. After classification of cystic lesions into EPVS or CLI, two readers assessed linear signs on T2WI and TOF MRA. We compared the prevalence and the diagnostic performance of linear signs. RESULTS: Among 46 EPVS and 51 CLI, 84 lesions (86.6%) were in basal ganglia. The prevalence of T2 and TOF linear signs was significantly higher in the EPVS than in the CLI (P < .001). For the diagnosis of EPVS, T2 and TOF linear signs showed high sensitivity (> 80%). TOF linear sign showed significantly higher specificity (100%) and accuracy (92.8% and 90.7%) than T2 linear sign (P < .001). CONCLUSIONS: T2 and TOF linear signs were more frequently observed in EPVS than CLI. They showed high sensitivity in differentiation of them, especially for basal ganglia. TOF sign showed higher specificity and accuracy than T2 sign. KEY POINTS: • Linear sign is a suggestive feature of EPVS. • Time-of-flight magnetic resonance angiography can reveal the lenticulostriate artery within perivascular spaces. • Linear sign helps differentiation of EPVS and CLI, especially in basal ganglia.

Cerebral small vessel disease and post-stroke cognitive impairment.

Cerebral small vessel disease (CSVD) refers to a group of pathological processes with multifarious etiologies that affect the small arteries, arterioles, venules, and capillaries of the brain. Features seen on neuroimaging include white matter hyperintensities, lacunar infarction, cerebral microbleeds, brain atrophy, microinfarcts and enlarged perivascular spaces (EPVS). CSVD gives rise to one in five strokes worldwide and is a leading cause of cognitive impairment and dementia, especially in the elderly. Post-stroke cognitive impairment (PSCI) is one of the most common subtypes of cognitive impairment. The underlying mechanisms of PSCI are not known in detail. A growing body of evidence has been suggesting that CSVD plays an important role in the pathogenesis of PSCI. This article reviews the advances in research on the relationship between CSVD and PSCI.

Baseline characteristic of patients presenting with lacunar stroke and cerebral small vessel disease may predict future development of depression.

OBJECTIVE: Cerebral small vessel disease (SVD) is associated with late-onset depression and increases the risk for depression after stroke. We aimed to investigate baseline predictors of depression after long-term follow-up in patients with SVD, initially presenting with first-ever lacunar stroke, free of depression and cognitive impairment. METHODS: A total of 294 patients with SVD were evaluated 3-5 years after the qualifying event. We analyzed baseline demographic data, vascular risk factors, functional status expressed as a score on modified Rankin Scale (mRS), cognitive status, presence of depression, total number of lacunar infarcts and severity of white matter hyperintensities (WMH) on MRI with Age-Related White Matter Changes scale total score (tARWMC) and Fazekas scale periventricular and deep subcortical scores. RESULTS: On follow-up, depression was registered in 117 (39.8%) SVD patients. At the baseline, patients with depression compared with non-depressed were older (64.4 vs 60.9 years; p = 0.007), had higher mRS score (2.8 ± 0.7 vs 1.5 ± 0.7; p < 0.0001) and had more severe lesions on MRI scales (p < 0.0001 for all parameters). On follow-up, depressed patients more frequently exhibited cognitive decline (75.2% depressed vs 56.5% non-depressed; p = 0.003). No difference was detected in risk factor frequency between groups. Multivariate Cox regression analysis adjusted by age and gender revealed independent predictors of depression: baseline mRS >2 (HR 2.17, 95%CI 1.74-2.72; p < 0.0001) and tARWMC (HR 1.05, 95%CI 1.02-1.09; p = 0.005), and cognitive decline on follow-up (HR 1.80, 95%CI 1.12-2.89; p = 0.015). CONCLUSIONS: Baseline functional status and severity of WMH and development of cognitive decline predict the occurence of late-onset depression in patients with SVD.

Neuroimaging markers for early neurologic deterioration in single small subcortical infarction.

BACKGROUND AND PURPOSE: Early neurological deterioration (END) occurs in ≥20% of single small subcortical infarctions (SSSIs; axial diameter ≤20 mm in the perforator territories) and deters functional recovery. Both microvasculopathies and atherosclerosis have been proposed to independently contribute to the occurrence of END in SSSI cases. We hypothesized that the occurrence of END in SSSIs differs according to the pathological process. METHODS: We collected data from 587 patients with SSSI within 48 hours of onset from a prospective stroke registry containing 4961 case records. Independent reviewers, blinded to END information, rated neuroimaging characteristics, including relevant artery stenosis (0% to 50% stenosis of the adjacent arteries on magnetic resonance angiography), branch atheromatous lesions (≥4 consecutive axial cuts or extensions from the basal surface of the pons), white matter hyperintensities, old lacunar infarctions, and cerebral microbleeds. RESULTS: END occurred in 79 (13.5%) cases, including 6 recurrences, 68 progressions, 1 symptomatic hemorrhagic transformation, 1 others, and 3 unknowns. END increased the National Institutes of Health Stroke Scale score by 2.3±1.4 points. Patients with END showed higher frequencies of modified Rankin Scale scores of 3 to 6 after 3 months compared with patients without END (49% versus 23%). Patients with relevant artery stenosis (adjusted odds ratio, 1.91; 95% confidence interval, 1.13-3.21) and branch atheromatous lesions (adjusted odds ratio, 2.98; 95% confidence interval, 1.80-4.93) had significantly higher odds of exhibiting END. However, such an association was not detected with small vessel disease markers. CONCLUSIONS: Our analysis indicated a potential contribution of the localized atherosclerotic process to END in SSSIs. Precautionary measures might be used for SSSIs suggestive of atherosclerotic pathologies.

Incidence and survival of lacunar infarction in a southern Chinese population: A 7-year prospective study.

OBJECTIVE: Little attention has been paid to the epidemiological characteristics of lacunar infarction (LAC) in China before. This study aimed to examine the incidence and survival of LAC in a southern Chinese population. METHODS: From 2004-2010 in Changsha, two communities with a registered population of ∼100 000 were selected and data from first-ever ischaemic stroke (IS) cases were prospectively collected. Then the epidemiological characteristics of LAC and non-LAC were evaluated. RESULTS: During the study period, the age-standardized incidence increased at an annual rate of 0.7% (p < 0.001) for LAC and 2.0% (p < 0.001) for non-LAC. The mean annual age-standardized incidence of LAC and non-LAC was 28.2/100 000 and 45.0/100 000, respectively. Compared with non-LAC patients, the prevalence of hypertension, diabetes and hyperlipidemia was significantly higher in patients with LAC (p < 0.05). Although the 30-day fatality rate was significantly lower in patients with LAC than non-LAC (0.5% vs. 14.9%, p < 0.001), there was no significant difference in survival between the two groups (96.7% vs. 95.2%, p = 0.203) after excluding the patients who died within 1 year of stroke onset. CONCLUSION: LAC is a common stroke sub-type in southern China and the long-term prognosis is not benign.

Clinical correlates of infarct shape and volume in lacunar strokes: the Secondary Prevention of Small Subcortical Strokes trial.

BACKGROUND AND PURPOSE: Infarct size and location are thought to correlate with different mechanisms of lacunar infarcts. We examined the relationship between the size and shape of lacunar infarcts and vascular risk factors and outcomes. METHODS: We studied 1679 participants in the Secondary Prevention of Small Subcortical Stroke trial with a lacunar infarct visualized on diffusion-weighted imaging. Infarct volume was measured planimetrically, and shape was classified based on visual analysis after 3-dimensional reconstruction of axial MRI slices. RESULTS: Infarct shape was ovoid/spheroid in 63%, slab in 12%, stick in 7%, and multicomponent in 17%. Median infarct volume was smallest in ovoid/spheroid relative to other shapes: 0.46, 0.65, 0.54, and 0.90 mL, respectively (P<0.001). Distributions of vascular risk factors were similar across the 4 groups except that patients in the ovoid/spheroid and stick groups were more often diabetic and those with multicomponent had significantly higher blood pressure at study entry. Intracranial stenosis did not differ among groups (P=0.2). Infarct volume was not associated with vascular risk factors. Increased volume was associated with worse functional status at baseline and 3 months. Overall, 162 recurrent strokes occurred during an average of 3.4 years of follow-up with no difference in recurrent ischemic stroke rate by shape or volume. CONCLUSIONS: In patients with recent lacunar stroke, vascular risk factor profile was similar among the different infarct shapes and sizes. Infarct size correlated with worse short-term functional outcome. Neither shape nor volume was predictive of stroke recurrence. CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT00059306.

Visit-to-visit systolic blood pressure variability predicts all-cause and cardiovascular mortality after lacunar infarct.

BACKGROUND AND PURPOSE: Both blood pressure (BP) and its variability (BPV) are established risk factors for development of atherosclerotic disease and are associated with an increased risk for cardiovascular and all-cause mortality. The prognostic implications of outpatient clinic visit-to-visit BPV amongst patients with lacunar infarction are nevertheless unknown. METHODS: The clinical outcome of 281 patients with lacunar infarction was prospectively followed up. The average BP and BPV, as determined by the standard deviation of the systolic and diastolic BP, were recorded during a mean 13 ± 6 outpatient clinic visits. RESULTS: The mean age of the population was 70 ± 10 years. After a mean 78 ± 18 months follow-up, 65 patients died (23%), 31% (20/65) due to cardiovascular causes; 14% and 7% developed recurrent stroke and acute coronary syndrome. After adjusting for age, sex, mean systolic and diastolic BP, cardiovascular risk factors and comorbidities, patients with a systolic BPV of the third tertile had significantly higher risk of all-cause mortality [hazard ratio (HR) 1.97, 95% confidence interval (CI) 1.02-3.80, P = 0.04) and cardiovascular mortality (HR 7.64, 95% CI 1.65-35.41, P < 0.01) than those with systolic BPV of the first tertile. Nevertheless, systolic BPV did not predict recurrent stroke or acute coronary syndrome. Diastolic BPV did not predict various adverse clinical outcomes. CONCLUSIONS: Visit-to-visit systolic BPV predicts long-term all-cause and cardiovascular mortality after lacunar infarct, independent of conventional risk factors including average BP control.