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Lacunes or lacunar infarcts are small fluid-filled cavities associated with cerebral small vessel disease (cSVD). They contribute to the development of lacunar stroke, dementia, and gait impairment. The identification of lacunes is of great significance in elucidating the pathophysiological mechanism of cSVD. This paper proposes a semi-automated 3D multi-scale residual convolutional network (3D ResNet) for lacunar infarcts detection, which can learn global representations of the anatomical location of lacunes using two multi-scale magnetic resonance image modalities. This process requires minimal user intervention by passing the potential suspicious lacunes into the network. The proposed network is trained, validated, and tested using five-fold cross-validation using data, including 696 lacunes, from 288 subjects. We also present experiments on various combinations of multi-scale inputs and their effect on extracting global context features that directly influence identification performance. The proposed system shows its capability to differentiate between true lacunes and lacune mimics, providing supportive interpretations for neuroradiologists. The proposed 3D multi-scale ResNet identifies lacunar infarcts with a sensitivity of 96.41%, a specificity of 90.92%, an overall accuracy of 93.67%, and an area under the receiver operator characteristic curve (AUC) of 93.67% over all fold tests. The proposed system also achieved a precision of 91.40% and an average number of FPs per subject of 1.32. The system may be feasible for clinical use by supporting decision-making for lacunar infarct detection.

Introduction and Purpose: Cerebral amyloid angiopathy (CAA) can be observed in patients with progressive supranuclear palsy (PSP), though to a lesser degree than in Alzheimer&rsquo, s disease. The present post-mortem 7.0-tesla magnetic resonance imaging (MRI) evaluates whether CAA has an influence on the degree of hippocampal atrophy (HA) and on the incidence of associated micro-infarcts (HMIs) and cortical micro-bleeds (HMBs). Material and Methods: Eight brains with PSP-CAA were compared to 20 PSP brains without CAA. In addition to the neuropathological examination, the hippocampus was evaluated on the most representative coronal section with T2 and T2*-weighted MRI sequences. The average degree of HA was determined in both groups. The incidence of HMIs and HMBs was also compared as well as the frequency of cortical micro-infarcts (CoMIs) and cortical micro-bleeds (CoMBs) in the hemispheric neocortex. Results: The neuropathological examination showed a higher incidence of lacunar infarcts in the PSP-CAA brains compared to the PSP ones. With magnetic resonance imaging (MRI), the severity of HA and the incidence of HMIs and HMBs was similar between both groups. Additionally, the frequency of CoMIs and CoMBs in the neocortex was comparable. Conclusions: The association of CAA in PSP brains has no influence on the degree of HA and on the incidence of the small cerebrovascular lesions in the hippocampus as well as in the neocortex.

Most studies in literature about the occurrence of the so-called vascular epilepsy suggest that this complication is an episodic and relatively rare event mostly due to clinical conditions related to haemorrhagic ictus while chronic vascular disease (multifocal vascular encephalopathy, vasculopathy with lacunar infarcts or minor stroke and ischemic strokes) is not usually considered as risk factors for the onset of secondary epilepsy. Furthermore, the epilepsy of the elderly is often ascribed to the atrophy of the brain tissues linked to both age and chronic hypoxia induced by Atherosclerosis (ATS) or a complication of pharmacological therapies in the elderly (anticholinesterases, neuroleptics, anticoagulants). In fact, in our clinical and practical experience in the district outpatients clinic and home care center, numerous clinical cases have been subject to diagnosis and treatment of late epilepsy following an ischemic stroke. In this study we had thepurpose to describe our experience of occurrence of epileptic complications in patients with morewide Cerebrovascular Disease (CVD) patterns. We studied a group of 15 patients (8 Male and 7 Female) affected by CVD and by recent recently onset epilepsy. Our study found that Cerebrovascular disease CVD constitutes a significant risk factor for secondary epilepsy in the groups with elder age even though younger subjects can be involved after being affected by relevant cerebrovascular events. In opposition to the opinion assumed in common clinical practice an important part of these causal events are ischemic and non-haemorrhagic as previously known.

Insulin resistance and muscle weakness are risk factors for silent lacunar infarcts (SLI), but it is unclear whether they are still independent risk factors when adjusted for each other. In addition, the effect of their combination on SLI is completely unknown. We evaluated SLI, insulin sensitivity, and knee extensor muscle strength by magnetic resonance imaging, PREDIM, and dynamometer, respectively, in 1531 elderly people aged 65–84 years living in an urban area of Tokyo. Among the study subjects, 251 (16.4%) had SLI. Impaired insulin sensitivity (High; 1.00 [reference], Medium; 1.53 [95% confidence interval (CI) 0.94–2.48], Low; 1.86 [1.02–3.39], p for trend 0.047) and reduced muscle strength (High; 1.00 [reference], Medium; 1.40 [0.98–2.02], Low; 1.49 [1.04–2.15], p for trend 0.037) were independently associated with increased risk for SLI in the fully adjusted model. In terms of combined, subjects classified as having the lowest insulin sensitivity and lowest strength were 4.33 times (95% CI 1.64–11.45) more likely to have a SLI than those classified as having the highest insulin sensitivity and highest strength. Impaired insulin sensitivity and reduced muscle strength were independently associated with higher risk of SLI in elderly subjects, and their combination synergistically increased this risk.

Chorea‑hemiballismus is the most common movement disorder, and it commonly results from vascular lesions in the subthalamic nucleus. Rarely, it can result from lacunar infarcts. Here is illustrated a 95‑year‑old male with sudden‑onset left-sided chorea‑hemiballismus of 2 weeks, without any other neurological deficit, who was not a diabetic patient and had no form of acidosis or electrolyte abnormality. Computerized tomogram, serial 32 slides pre‑ and post‑contrast images showed small non-enhancing, hypodense foci within the right frontal subcortical region adjacent to the frontal horn of the right lateral ventricle as well as within the lentiform nucleus. There were no mass effects seen. A diagnosis of hemiballismus from subcortical lacunar infarct was made. The hemiballismus was controlled after 2 weeks of haloperidol and clonazepam therapy, among others, with a substantial reduction in the abnormal movements. Hemiballismus attributable to subcortical lacunar infarcts though rare was presented. Keywords: Hemiballismus, lacunar infarcts, lentiform nucleus, Nigeria, subcortical infarcts, subthalamic nucleus

We evaluated the predictive value of several clinical, radiological and laboratory parameters on the risk of predict intracranial hemorrhage (ICH) in patients with atrial fibrillation (AF). We conducted a case-control study on a consecutive hospital based series of patients with AF and ICH. A random sample of subjects with AF without ischemic or hemorrhagic stroke was selected from the same hospital in the same period to perform as the control group, with a ratio of two controls per case. All patients underwent the same evaluation protocol. Patients without neuroimaging exams were excluded. During the study period we identified 37 subjects with AF and ICH. 74 subjects without stroke events were randomly chosen among subjects with AF. Among cases 56.8% were female; mean age was 83.1 years. Patients with ICH were more often on anticoagulant therapy (75.7%), compared with controls (45.9%; p = 0.0002). On CT scans, cases had a greater severity of leukoaraiosis at the Blennow scale (p

Funder: National Institute for Health Research; Id: http://dx.doi.org/10.13039/501100000272, Funder: Biotechnology and Biological Sciences Research Council; Id: http://dx.doi.org/10.13039/501100000268, BACKGROUND: Cerebral small vessel disease (SVD) leads to reduced quality of life (QOL), but the mechanisms underlying this relationship remain unknown. This study investigated multivariate relationships between radiological markers of SVD and domain-specific QOL deficits, as well as potential mediators, in patients with SVD. METHODS: Clinical and neuroimaging measures were obtained from a pooled sample of 174 SVD patients from the St. George's Cognition and Neuroimaging in Stroke and PRESsure in established cERebral small VEssel disease studies. Lacunes, white matter hyperintensities, and microbleeds were defined as radiological markers of SVD and delineated using MRI. QOL was assessed using the Stroke-Specific Quality of Life Scale. Multivariate linear regression was used to determine whether SVD markers were associated with domain-specific QOL deficits. Significant associations were further investigated using mediation analysis to examine whether functional disability or cognition was potential mediators. RESULTS: Multivariate regression analyses revealed that lacunes were associated with total QOL score (β = -8.22, p = .02), as well as reductions in mobility (β = -1.41, p = .008) and language-related subdomains (β = -0.69, p = .033). White matter hyperintensities and microbleeds showed univariate correlations with QOL, but these became nonsignificant during multivariate analyses. Mediation analyses revealed that functional disability, defined as reduced activities of daily living, and executive function, partially mediated the relationship between lacunes and total QOL, as well as mobility-related QOL, but not language-related QOL. CONCLUSIONS: Lacunar infarcts have the most detrimental effect on QOL in SVD patients, particularly in the mobility and language-related subdomains. These effects may be partially explained by a reduction in activities of daily living. These results may inform targeted interventions to improve QOL in patients with SVD.

Background: Previous studies showed that insulin resistance and reduced muscle strength are risk factors for silent lacunar infarcts, but it is unclear whether they are still independent risk factors when adjusted for each other. In addition, the effect of their combination on silent lacunar infarcts is completely unknown.Methods: We evaluated silent lacunar infarcts, insulin sensitivity, and knee extensor muscle strength by magnetic resonance imaging, PREDIM (an index for insulin sensitivity), and dynamometer, respectively, in 1531 elderly people aged 65–84 years living in an urban area of Tokyo. Results: Among the study subjects, 251 (16.4%) had silent lacunar infarcts. Impaired insulin sensitivity (High; 1.00 [reference], Medium; 1.53 [95% confidence interval (CI): 0.94-2.48], Low; 1.86 [95%CI: 1.02-3.39], p for trend 0.047) and reduced muscle strength (High; 1.00 [reference], Medium; 1.40 [95%CI: 0.98-2.02], Low; 1.49 [95%CI: 1.04-2.15], p for trend 0.037) were independently associated with increased risk for silent lacunar infarcts in the fully adjusted model. In terms of combined, subjects classified as having the lowest insulin sensitivity and lowest strength were 4.33 times (95%CI: 1.64-11.45) more likely to have a silent lacunar infarct than those classified as having the highest insulin sensitivity and highest strength.Conclusions: Impaired insulin sensitivity and reduced muscle strength were independently associated with higher risk of silent lacunar infarcts in elderly subjects, and their combination synergistically increased this risk.

Background: Perforator disease caused by parent artery atheromatous disease is one of the mechanisms implicated in the pathogenesis of lacunar infarcts, but there is limited data on its prevalence. We sought to determine the prevalence of parent vessel atheromatous disease in patients with lacunar infarcts. Methods: This is a retrospective study of consecutive patients with lacunar strokes admitted to NYU Langone Medical Center and Brown University from 2017-2019. Lacunar infarct was defined as subcortical infarct 50%) in the parent vessel and no cardioembolic source. Non-invasive imaging (CTA or MRA) was reviewed by a neuroradiologist or a vascular neurologist to determine the presence or absence of stenosis (< 50%) or luminal irregularity without stenosis in the stem artery segment at the location of the perforator corresponding to the infarct. Patients were divided into two groups: luminal irregularity/stenosis vs. none. We compared clinical and radiographic characteristics and rates of neurological deterioration between the two groups. Results: Among 208 patients with lacunar infarcts (mean age 68.9±11.9 years, 40.9% women, 61.1% White, 13.9% Black, and 12.5% Hispanic), 42 (20.2%) had luminal stenosis and 90 (43.3%) had luminal irregularity without stenosis. Baseline characteristics and prevalence of risk factors were similar between the two groups. Patients with luminal irregularity/stenosis had longer median infarct diameter (10.6 mm vs 8.7 mm, p=0.007). Other imaging variables such as the presence of prior lacunar infarcts and white matter disease burden assessed by Fazekas Score were not significantly different between the two groups. The rate of any neurological deterioration after admission was similar between the two groups (22.7% vs. 15.8%, p=0.283). Conclusion: In this multi-ethnic population, nearly two-thirds of patients with a lacunar infarct were found to have luminal irregularity or stenosis in the parent artery corresponding to the infarct, implying a potential atherosclerotic mechanism. Future studies are needed using advanced imaging of the stem artery to define plaque characteristics which may help determine the underlying mechanism.

Background Cerebral small vessel disease (SVD) leads to reduced quality of life (QOL), but the mechanisms underlying this relationship remain unknown. This study investigated multivariate relationships between radiological markers of SVD and domain‐specific QOL deficits, as well as potential mediators, in patients with SVD. Methods Clinical and neuroimaging measures were obtained from a pooled sample of 174 SVD patients from the St. George's Cognition and Neuroimaging in Stroke and PRESsure in established cERebral small VEssel disease studies. Lacunes, white matter hyperintensities, and microbleeds were defined as radiological markers of SVD and delineated using MRI. QOL was assessed using the Stroke‐Specific Quality of Life Scale. Multivariate linear regression was used to determine whether SVD markers were associated with domain‐specific QOL deficits. Significant associations were further investigated using mediation analysis to examine whether functional disability or cognition was potential mediators. Results Multivariate regression analyses revealed that lacunes were associated with total QOL score (β = −8.22, p = .02), as well as reductions in mobility (β = −1.41, p = .008) and language‐related subdomains (β = −0.69, p = .033). White matter hyperintensities and microbleeds showed univariate correlations with QOL, but these became nonsignificant during multivariate analyses. Mediation analyses revealed that functional disability, defined as reduced activities of daily living, and executive function, partially mediated the relationship between lacunes and total QOL, as well as mobility‐related QOL, but not language‐related QOL. Conclusions Lacunar infarcts have the most detrimental effect on QOL in SVD patients, particularly in the mobility and language‐related subdomains. These effects may be partially explained by a reduction in activities of daily living. These results may inform targeted interventions to improve QOL in patients with SVD., Fernando et al. investigate associations between radiological markers of cerebral small vessel disease (SVD) and subdomains of quality of life (QOL). In a pooled sample of SVD patients, they find that lacunes lead to reductions in total QOL, as well as mobility and language‐related QOL, and explore potential mediating variables. These results suggest the possibility of targeted interventions to improve QOL in SVD patients.

Cerebral small vessel disease (SVD) is a major health burden, yet the pathophysiology remains poorly understood with no effective treatment. Since much of SVD develops silently and insidiously, non-invasive neuroimaging such as MRI is fundamental to detecting and understanding SVD in humans. Several relevant SVD rodent models are established for which MRI can monitor in vivo changes over time prior to histological examination. Here, we critically review the MRI methods pertaining to salient rodent models and evaluate synergies with human SVD MRI methods. We found few relevant publications, but argue there is considerable scope for greater use of MRI in rodent models, and opportunities for harmonisation of the rodent-human methods to increase the translational potential of models to understand SVD in humans. We summarise current MR techniques used in SVD research, provide recommendations and examples and highlight practicalities for use of MRI SVD imaging protocols in pre-selected, relevant rodent models. Electronic supplementary material The online version of this article (10.1007/s12975-020-00843-8) contains supplementary material, which is available to authorised users.

Silent lacunar infarcts (SLI) are often incidentally found on brain MRI scans in asymptomatic elderly people, and are associated with the future onset of stroke and dementia. However, the risk factors for SLI have not been fully elucidated yet. We recently found that reduced muscle strength is a risk factor for SLI. Systemic insulin sensitivity (IS) that reflects the metabolic function of muscles could also be a risk factor for SLI; however, interactive effect of IS and muscle strength on SLI is totally unknown. Here, we evaluated SLI, recently established index of IS (PREDIM) and knee extensor muscle strength by MRI, oral glucose tolerance test, and dynamometer, respectively on 1,531 elderly people aged 65-84 years living in an urban area of Tokyo. The subjects were categorized into 3 groups based on the standard deviation of PREDIM and the tertiles of muscle strength, respectively, then categorized into 9 groups by their combination, then we estimated odd ratios for SLI by logistic regression analysis. Among the study subjects, we found 251 (16.4%) subjects had silent lacunar infarcts. IS was weakly correlated to muscle strength (r=0.185, p=0.001). Impaired IS [High; 1.00 (reference), Medium; 1.53 (95%CI: 0.94-2.48), Low; 1.85 (95%CI: 1.02-3.38), p for trend 0.047] and reduced muscle strength [High; 1.00 (reference), Medium; 1.42 (95%CI: 0.99-2.04), Low; 1.51 (95%CI: 1.05-2.16), p for trend 0.034] were independently associated with increased risk for SLI in the fully adjusted model. In terms of interactive association, subjects categorized in the lowest IS and muscle strength had 4.4 fold (95%CI: 1.67-11.64) higher risk for SLI compared with those categorized in both are the highest. In summary, reduced muscle strength and IS were independently associated with higher risk for SLI in elderly subjects, and combination of both was synergistically elevated the risk for SLI. Disclosure Y. Someya: None. Y. Tamura: Advisory Panel; Self; Astellas Pharma Inc. Research Support; Self; Kowa Company, Ltd. Speaker’s Bureau; Self; Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd. H. Kaga: None. D. Sugimoto: None. S. Kadowaki: None. R. Suzuki: None. R. Kawamori: None. H. Watada: Advisory Panel; Self; Abbott, Ajinomoto, Astellas Pharma Inc., Boehringer Ingelheim Pharmaceuticals, Inc., Fuji Film, Janssen Pharmaceuticals, Inc., Kowa Company, Ltd., Kyowa Hakko Kirin Co., Ltd., Mitsubishi Tanabe Pharma Corporation, Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Sanofi-Aventis, Takeda Pharmaceutical Company Limited, Terumo Medical Corporation. Research Support; Self; Astellas Pharma Inc., Bayer Yakuhin, Ltd., Boehringer Ingelheim Pharmaceuticals, Inc., Daiichi Sankyo, Eli Lilly Japan K.K., Kissei Pharmaceutical Co., Ltd., Kowa Company, Ltd., Kyowa Hakko Kirin Co., Ltd., Merck Sharp & Dohme Corp., Mitsubishi Tanabe Pharma Corporation, Novartis Pharma K.K., Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Otsuka Pharmaceutical Co., Ltd., Pfizer Japan Inc., Sanofi-Aventis, Sanwa Kagaku Kenkyusho, Shionogi & Co., Ltd., Sumitomo Dainippon Pharma Co., Ltd., Sumitomo Dainippon Pharma Co., Ltd., Taisho Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited, Teijin Pharma Limited, Yakult. Speaker’s Bureau; Self; Astellas Pharma Inc., AstraZeneca, Bayer Yakuhin, Ltd., Boehringer Ingelheim Pharmaceuticals, Inc., Daiichi Sankyo, Eli Lilly Japan K.K., Kissei Pharmaceutical Co., Ltd., Kowa Company, Ltd., Kyowa Hakko Kirin Co., Ltd., Merck Sharp & Dohme Corp., Mitsubishi Tanabe Pharma Corporation, Novartis Pharmaceuticals Corporation, Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Sanofi-Aventis, Sanwa Kagaku Kenkyusho, Sumitomo Dainippon Pharma Co., Ltd., Takeda Pharmaceutical Company Limited. Funding Strategic Research Foundation at Private Universities (S1411006); Japan Society for the Promotion of Science (18H03184); Mizuno Sports Promotion Foundation; Mitsui Life Social Welfare Foundation

Central retinal artery occlusion (CRAO) is an ophthalmic emergency. It occurs when central retinal artery gets occluded. We present a case of a 34-years-old male, alcoholic and a smoker presenting with sudden loss of vision of right eye. Fundus examination revealed a picture of CRAO. On further neuroimaging, a silent acute to subacute lacunar infarcts were found.

Cerebral microinfarcts are small lesions that are presumed to be ischaemic. Despite the small size of these lesions, affected individuals can have hundreds to thousands of cerebral microinfarcts, which cause measurable disruption to structural brain connections, and are associated with dementia that is independent of Alzheimer's disease pathology or larger infarcts (ie, lacunar infarcts, and large cortical and non-lacunar subcortical infarcts). Substantial progress has been made with regard to understanding risk factors and functional consequences of cerebral microinfarcts, partly driven by new in-vivo detection methods and the development of animal models that closely mimic multiple aspects of cerebral microinfarcts in human beings. Evidence from these advances suggests that cerebral microinfarcts can be manifestations of both small vessel and large vessel disease, that cerebral microinfarcts are independently associated with cognitive impairment, and that these lesions are likely to cause damage to brain structure and function that extends beyond their actual lesion boundaries. Criteria for the identification of cerebral microinfarcts with in-vivo MRI are provided to support further studies of the association between these lesions and cerebrovascular disease and dementia.

Objective Cerebral small vessel disease (SVD) is inversely associated with cognitive performance. However, whether the total SVD score is a better predictor of poor cognitive performance than individual signatures of SVD is inconclusive. We aimed to estimate the combined and independent predictive power of these MRI findings. Methods Atahualpa residents aged ≥60 years underwent brain MRI. Cognitive performance was measured by the Montreal Cognitive Assessment (MoCA). The presence of moderate-to-severe white matter hyperintensities, deep cerebral microbleeds, lacunar infarcts, and >10 enlarged perivascular spaces was added for estimating the total SVD score ranging from 0 to 4 points. Montreal Cognitive Assessment predictive models were fitted to assess how well the total SVD score or each of its components predicts cognitive performance. Results Of 351 eligible candidates, 331 (94%) were included. The total SVD score was 0 points in 202 individuals (61%), 1 point in 67 (20%), 2 points in 40 (12%), 3 points in 15 (5%), and 4 points in seven (2%). A generalized lineal model showed an inverse relationship between the total SVD score and the MoCA (p = 0.015). The proportion of variance in the MoCA score explained by the SVD score was 32.8% (R2 = 0.328). This predictive power was similar for white matter hyperintensities (R2 = 0.306), microbleeds (R2 = 0.313), lacunar infarcts (R2 = 0.323), and perivascular spaces (R2 = 0.313). Conclusions This study shows a significant association between the SVD score and worse cognitive performance. The SVD score is a predictor of poor cognitive performance. This predictive power is not better than that of isolated neuroimaging signatures of SVD. Copyright © 2017 John Wiley & Sons, Ltd.

Frailty is a common syndrome in older individuals that is associated with poor cognitive outcome. The underlying brain correlates of frailty are unclear. The aim of this study was to investigate the association between frailty and MRI features of cerebral small vessel disease in a group of non-demented older individuals. We included 170 participants who were classified as frail (n = 30), pre-frail (n = 85) or non-frail (n = 55). The association of frailty and white matter hyperintensity volume and shape features, lacunar infarcts and cerebral perfusion was investigated by regression analyses adjusted for age and sex. Frail and pre-frail participants were older, more often female and showed higher white matter hyperintensity volume (0.69 [95%-CI 0.08 to 1.31], p = 0.03 respectively 0.43 [95%-CI: 0.04 to 0.82], p = 0.03) compared to non-frail participants. Frail participants showed a non-significant trend, and pre-frail participants showed a more complex shape of white matter hyperintensities (concavity index: 0.04 [95%-CI: 0.03 to 0.08], p = 0.03; fractal dimensions: 0.07 [95%-CI: 0.00 to 0.15], p = 0.05) compared to non-frail participants. No between group differences were found in gray matter perfusion or in the presence of lacunar infarcts. In conclusion, increased white matter hyperintensity volume and a more complex white matter hyperintensity shape may be structural brain correlates of the frailty phenotype.

Supplemental Digital Content is available in the text., Background and Purpose— Cerebral small vessel disease is characterized by a wide range of focal and global brain changes. We used a magnetic resonance imaging segmentation tool to quantify multiple types of small vessel disease–related brain changes and examined their individual and combined predictive value on cognitive and functional abilities. Methods— Magnetic resonance imaging scans of 560 older individuals from LADIS (Leukoaraiosis and Disability Study) were analyzed using automated atlas- and convolutional neural network–based segmentation methods yielding volumetric measures of white matter hyperintensities, lacunes, enlarged perivascular spaces, chronic cortical infarcts, and global and regional brain atrophy. The subjects were followed up with annual neuropsychological examinations for 3 years and evaluation of instrumental activities of daily living for 7 years. Results— The strongest predictors of cognitive performance and functional outcome over time were the total volumes of white matter hyperintensities, gray matter, and hippocampi (P

Lambl’s excrescences (LE) are rare cardiac structures. They are associated with catastrophic thromboembolic and coronary events. Despite resulting in such important events, 2D echocardiographic imaging modalities may overlook LE owing to very thin cardiac structures. So, 3D echocardiographic imaging modalities may fully offer this cardiac mass and provide us to more accurately guess the complication rate related to LE due to the fact that 3D echocardiographic imaging techniques have higher spatial resolution and are not based on the geometric assumption. Indeed, another benefit of 3D echocardiographic imaging modalities in this population is that these imaging modalities clearly provide the relationship to adjacent structures of LE and its movement over a cardiac cycle in 3D space. In our case report, we aim to present the usefulness of 3D echocardiography as a modality to clearly offer all features of LE, furthermore to give valuable information about management in patients with thromboembolic events leading to LE.

We evaluated a prospective cohort of 150 patients under observation in our centre for lacunar strokes. The purpose of this study was to investigate if lacunar stroke of varying size, shape and locations had different risk factors between them and possibly different mechanisms and causes.150 patients with a lacunar stroke were included in the present study. Infarcts were classified by size, shape and location. We evaluated the correlation between several risk factors of stroke and the radiological characteristics of the infarcts.Older age was associated with the presence of a basal ganglia lesion (p0.001) and with the presence of a smaller lesion (trend to statistical significance, p = 0.07). Patients with infarcts15 mm had higher NIHSS score at admission (p 0.01).The different subtypes of lacunar infarcts have distinct pathogenesis. Further studies, with a larger numbers of patients, are necessary to confirm our data.

To investigate the alterations of basal ganglia (BG)-cortical structural and functional connectivity induced by subcortical silent lacunar infarct (SLI), and their associations with cognitive impairment in SLI subjects. All participants were recruited from communities, including 30 subcortical SLIs and 30 age-, gender-, and education-matched healthy controls. The structural and functional connectivity of BG-cortical circuits using diffusion and resting-state functional magnetic resonance imaging data were obtained. Diffusion abnormalities of the white matter tracts connecting the BG and cortical areas were observed in SLI subjects, including the BG-lateral frontal, BG-orbital frontal, and BG-insula tracts. Multiple regions showed a reduced BG-cortical functional connectivity in SLI patients, including direct connectivities with the BG, such as the BG-limbic, BG-insula, and BG-frontal connectivities, and others that showed no direct causation with the BG, such as the insula-limbic, insula-parietal, and frontal-parietal connectivities. Coupling of structural and functional BG-cortical connectivity was observed in healthy controls but not in SLI patients. Significant correlations between structural and functional BG-cortical connectivity and cognitive performance were demonstrated in SLI patients, indicating the potential use of BG-cortical connectivities as MRI biomarkers to assess cognitive impairment. These findings suggest that subcortical SLIs can impair BG-cortical circuits, and these changes may be the pathological basis of cognitive impairment in SLI patients.

Purpose To characterize the orifices of lenticulostriate arteries (LSAs) in vivo by using three-dimensional (3D) time-of-flight magnetic resonance angiography (TOF-MRA) and to investigate the spatial relationship between LSA orifices and atherosclerotic plaques in patients with lacunar infarcts (LI). Method Seventeen healthy volunteers and fifteen patients with LI underwent 3D TOF-MRA and 3D vessel wall imaging (VWI) at 7 T. The orifices of LSAs and the locations of atherosclerotic plaques on MCA walls were categorized based on the involvement of the superior, inferior, ventral or dorsal sides of MCA wall. The distribution quadrants of LSA orifices on MCA walls were compared among different groups. Results Most orifices were located on the superior side of MCA firstly (46 of 95, 48.4%), followed by the dorsal side (22 of 95, 23.2%). In patients with LI, the visible numbers of ventral and inferior orifices on the ipsilateral side were significantly lower than healthy controls (p = 0.039 for ventral side, p = 0.002 for inferior side). Similarly, plaques occurred more frequently at the ventral (7 of 20, 35.0%) and the inferior (7 of 20, 35.0%) sides of MCA walls. Conclusions TOF-MRA at 7 T is capable of imaging orifices of LSA on MCA. In patients with LI, the decreased number of LSA orifices on the ventral and inferior sides corresponded with the distribution of MCA plaques. The results may indicate the vulnerability of LSA orifices in intracranial atherosclerosis, which was supposed to be the cause of LI in basal ganglia.

Lacunar syndromes are usually caused by small ischemic lesions called lacunar infarcts. However, non-lacunar infarcts account for about 20% of lacunar syndromes. The aim of this study was to identify clinical predictors of lacunar syndromes led by non-lacunar infarcts. The following single centre, observational study was conducted on an analysis of the “Perugia hospital-based Stroke Registry” database enrolling consecutive patients admitted with ischemic stroke during the period 2010–2017. We evaluated patient risk factors and clinical features linked to stroke syndrome (lacunar/non-lacunar) and to cerebral infarction (lacunar/non-lacunar). Lacunar syndromes were diagnosed in 478 (26.6%) out of 1796 patients. In 104 (21.1%) patients, lacunar syndromes were caused by non-lacunar infarcts. Lacunar syndromes with lacunar infarcts were primarily linked to diabetes (27.8% vs 16.3%) and obesity (7.7% vs 0.9%), while lacunar syndromes with non-lacunar infarcts were linked to a higher risk of atrial fibrillation (22.1% vs 9.4%) and higher National Institute of Health Stroke Scale scores on admission (mean 5.5 ± 3.7 vs 4.7 ± 2.8). On multivariate analysis, atrial fibrillation (OR 1.67, 95% CI 1.09–2.31; p = 0.002) and higher NIHSS (OR 1.12 for each point increase, 95% CI 1.09–1.15; p

Background In the list of named numerical neuro-ophthalmological syndromes, such as one-and-a-half syndrome and others, we report for the first time twenty-and-a-half syndrome, which is characterized by one-and-a-half syndrome with bilateral seventh and right fifth nerve palsy (1.5 + 7 + 7 + 5 = 20.5) in a patient with ischemic stroke. Case presentation A 45-year-old Asian Hindu woman presented with vomiting and imbalance of 1 day’s duration. She had left-sided ataxic hemiparesis with one-and-a-half syndrome with bilateral seventh and right fifth nerve palsy. Magnetic resonance imaging of her brain revealed acute non-hemorrhagic infarct in the right posterolateral aspect of pons and medulla, with normal brain vessels angiography. We described her disorder as twenty-and-a-half syndrome. She was put on antiplatelet therapy. Conclusions Twenty-and-a-half syndrome is reported for the first time. It is due to posterior circulation stroke; in our case, it was due to lacunar infarcts in the pons and medulla, manifesting as one-and-a-half syndrome with bilateral seventh and right fifth nerve palsy.

Cerebro vascular accident (CVA) is the third leading cause of death in developing countries. This disease has posed a great problem to the medical field as far as its treatment is concerned. Ayurveda can offer a lot in such conditions. This is a case study of an acute CVA. An acute CVA case was admitted on 23/05/2016 at 7.30 pm, with the complaints of loss of strength in the right side of the body, loss of speech, drowsiness since 2 days. On examination Glasgowcoma scale was 8/15 (E - 2, M- 1, V-2). Investigation i.e., Computed Tomography (CT) scan of head showed on 24/05/2016: Lacunar infarcts in the Right Frontal White matter and in the Pons at the Midline. It was diagnosed as Pitta Kapha Avruta Vataja Pakshaghata (Vaama). In this case various treatment procedures like cold water pouring over forehead, application of medicated paste on anterior frontanallae, application of Shathadhouta Ghrutha all over the body, nasal instillation etc. with oral medicines were adopted at various condition of the disease. There was a remarkable improvement in the subjective and objective clinical features.

Individuals with an abnormal ankle-brachial index (ABI) are four times more likely to have a silent lacunar infarct (SLI), but reliability of ABI in predicting the presence of these lesions has not been estimated yet. We compared two methods of calculating ABI to assess their reliability in predicting SLIs. Stroke-free Atahualpa residents aged ≥ 60 years underwent MRI of the brain and ABI determinations. Persons with ABI ≥ 1.4 were excluded. Using receiver operator characteristic curve analysis, we calculated the reliability of the traditional as well as an alternative ABI method to identify individuals with SLI. The traditional ABI uses the higher systolic pressure of either the dorsalis pedis or the posterior tibial arteries as the numerator, whereas the alternative ABI uses the lower pressure. Of the 247 participants, 38 (15%) had traditional and 95 (38%) had alternative ABIs ≤ 0.9. Twenty-one individuals had SLI. Traditional and alternative ABIs ≤ 0.9 identified 9 and 13 individuals with SLI, respectively. The traditional ABI had sensitivity of 42.9% (22.6–65.6%) and specificity of 87.2% (81.9–91.1%). The alternative ABI had sensitivity of 61.9% (38.6–81%) and specificity of 63.7% (57–69.9%). The area under the curve for the predictive value of SLI was 0.65 (0.54–0.76) for the traditional and 0.63 (0.52–0.74) for the alternative ABI ≤ 0.9. The ABI is moderately reliable for identifying candidates for MRI screening in studies assessing the burden of SLI in older adults. The traditional ABI seems to be more suitable for this purpose.

Mutations in type four collagens, specifically COL4A1 and COL4A2, have been associated with cerebral small vessel disease (SVD), defined as lacunar infarcts, deep intracerebral hemorrhages (ICH), and leukoaraiosis. We present a case of a man with recurrent cerebral infarcts, related to a novel COL4A2 mutation, the p.A1534S variant. Magnetic resonance imaging demonstrated multiple lacunar infarcts, numerous deep and lobar microhemorrhages and advanced leukoaraiosis. Evaluation for COL4A2 mutations should be considered when suspecting a genetic cerebral small vessel disease.

Nitrones (e.g. α-phenyl-N-tert-butyl nitrone; PBN) are cerebroprotective in experimental stroke. Free radical trapping is their proposed mechanism. As PBN has low radical trapping potency, we tested Sgk1 induction as another possible mechanism. PBN was injected (100 mg/kg, i.p.) into adult male rats and mice. Sgk1 was quantified in cerebral tissue by microarray, quantitative RT-PCR and western analyses. Sgk1+/+ and Sgk1−/− mice were randomized to receive PBN or saline immediately following transient (60 min) occlusion of the middle cerebral artery. Neurological deficit was measured at 24 h and 48 h and infarct volume at 48 h post-occlusion. Following systemic PBN administration, rapid induction of Sgk1 was detected by microarray (at 4 h) and confirmed by RT-PCR and phosphorylation of the Sgk1-specific substrate NDRG1 (at 6 h). PBN-treated Sgk1+/+ mice had lower neurological deficit ( p +/+ mice. PBN-treated Sgk1−/− mice did not differ from saline-treated Sgk1−/− mice. Saline-treated Sgk1−/− and Sgk1+/+ mice did not differ. Brain Sgk3:Sgk1 mRNA ratio was 1.0:10.6 in Sgk1+/+ mice. Sgk3 was not augmented in Sgk1−/− mice. We conclude that acute systemic treatment with PBN induces Sgk1 in brain tissue. Sgk1 may play a part in PBN-dependent actions in acute brain ischemia.

The imaging definition of lacunar infarcts is variable, particularly regarding their size and the presence of cavitation. We investigated the changes of diameter and evolution pattern of acute lacunar infarcts, and the factors associated with the evolution pattern. Patients with acute single subcortical hemispheric or brainstem ischemic lesions of penetrating arterial territories were included. Maximal diameters on initial diffusion-weighted image (DWI) and follow-up fluid-attenuated inversion recovery image (FLAIR), which performed > 12 months after initial DWI, were semi-automatically measured. Clinical characteristics were compared according to evolution patterns on follow-up FLAIR, classified as cavitated, focal lesion without cavitation, and disappeared. Five hundred nine patients were included. Mean time to follow-up was 31.3 ± 13.7 months. Mean diameter of acute lacunar lesions decreased from 12.9 ± 4.4 to 8.5 ± 4.8 mm during follow-up. Lesions of 58.2% patients remained as cavitated, 18.3% as focal lesion without cavitation, and 23.6% disappeared. Initial NIHSS score (p = 0.005), diameter of initial lesion (p

Background White matter hyperintensities ( WMHs ) are commonly asymmetric between hemispheres but for unknown reasons. We investigated asymmetric WMHs associated with lacunar infarcts. Methods and Results A total of 267 consecutive patients with small first‐ever supratentorial infarcts (≤20 mm) were included. None had a relevant vascular stenosis. WMH asymmetry was measured based on the hemispheric difference of a modified Scheltens scale score (≥3 defined as asymmetric). We analyzed the association of the hemispheric WMH asymmetry with old silent lacunar infarcts or acute lacunar infarcts. We compared lesion frequency maps between groups and generated t‐statistics maps. The mean age of patients was 64 years, and 63% were men. Asymmetric WMH was more than 3‐fold as frequent ( P WMHs , an acute lacunar infarct was more likely to be located in the left (versus right) hemisphere (74% versus 26%, P WMHs , an acute lacunar infarct was more likely to be located on the right (versus left) hemisphere (81% versus 19%, P WMHs was associated with acute and silent lacunes on the same side. Conclusions These are the first data to show that asymmetric WMH s are associated with both old silent lacunar infarcts and acute lacunar infarcts ipsilateral to the greatest WMH burden. This suggests that the hemisphere with relatively large WMHs is more vulnerable to ischemia.

We commend Loos et al in their investigation of associative factors pertaining to white matter hyperintensity progression and incident lacunar infarction among a cohort derived from 2 prospective observational studies in patients with minor ischemic stroke. Five-year follow-up magnetic resonance imaging data are provided.1 Incident lacunar infarction mainly occurred in the subcortical …

Impaired cerebrovascular reactivity precedes histological and clinical evidence of CADASIL in animal models. We aimed to more fully characterise peripheral and cerebral vascular function and reactivity in a cohort of adult CADASIL patients, and explore the associations of these with conventional clinical, imaging and neuropsychological measures. A total of 22 adults with CADASIL gave informed consent to participate in an exploratory study of vascular function in CADASIL. Clinical assessment, comprehensive vascular assessment, MRI and neuropsychological testing were conducted. We measured cerebral vasoreactivity with transcranial Doppler and arterial spin labelling MRI with hypercapnia challenge. Number and volume of lacunes, subcortical hyperintensity volume, microbleeds and normalised brain volume were assessed on MRI. Analysis was exploratory and examined the associations between different markers. Cerebrovascular reactivity measured by ASL correlated with peripheral vasoreactivity measured by flow mediated dilatation. Subjects with ≥5 lacunes were older, with higher carotid intima-media thickness and had impaired cerebral and peripheral vasoreactivity. Subjects with depressive symptoms, disability or delayed processing speed also showed a trend to impaired vasoreactivity. Impaired vasoreactivity and vascular dysfunction may play a significant role in the pathophysiology of CADASIL, and vascular assessments may be useful biomarkers of severity in both longitudinal and clinical trials.

Background and Aims In addition to overt stroke lesions, co-occurring covert lesions, including white matter hyperintensities (WMH) and covert lacunar infarcts (CLI), contribute to poststroke outcome. The purpose of this study was to examine the relationship between covert lesions, and motor and cognitive outcomes in individuals with chronic stroke. Methods Volumetric quantification of clinically overt strokes, covert lesions (periventricular and deep: pWMH, dWMH, pCLI, dCLI), ventricular and sulcal CSF (vCSF, sCSF), and normal appearing white (NAWM) and gray matter (NAGM) was performed using structural magnetic resonance imaging. We assessed motor impairment and function, and global cognition, memory, and other cognitive domains. When correlation analysis identified more than one MR parameter relating to stroke outcomes, we used regression modeling to identify which factor had the strongest impact. Results Neuropsychological and brain imaging data were collected from 30 participants at least 6 months following a clinically diagnosed stroke. Memory performance related to vCSF (r = −0.52, P = .004). The strongest predictor of nonmemory domains was pCLI (r2 = 0.28, P = .004). Motor impairment and function were most strongly predicted by the volume of stroke and NAWM (r2 = 0.36; P = .001), and dWMH (r2 = 0.39; P = .001) respectively. Conclusions Covert lesion type and location have important consequences for post-stroke cognitive and motor outcome. Limiting the progression of covert lesions in aging populations may enhance the degree of recovery post-stroke.

Aim: We aimed to investigate the association between reduced lung function and cerebral small vessel diseases via cranial magnetic resonance imaging (MRI) in the cross-sectional study of the general Japanese population. Methods: We recruited participants aged ≥ 40 years from the general population of a single city in Japan. We clarified the comorbidities and treatments, smoking habits, second-hand smoke exposure, current alcohol consumption, education level, exercise habits, and occupation. The pulmonary function test was performed to assess the forced expiratory volume in 1 second (FEV1) % predicted and forced vital capacity (FVC) % predicted values. Cranial MRI was performed to evaluate the white matter lesions (WMLs) and lacunar infarcts. We examined the association of the WMLs and lacunar infarcts with a 1-standard deviation (SD) lower in the FEV1 % predicted and FVC % predicted, on the basis of the smoking status. Results: A total of 473 men were examined. The association of WMLs and lacunar infarcts with the spirometry-based indices were significant only in never smokers. The association between lung function impairment and cerebral small vessel disease did not change after further adjusting for second-hand smoke exposure. Conclusion: In a community-based sample of Japanese men, we found an association between reduced lung function and WMLs and lacunar infarcts in never smokers.

Increasing evidence suggests that uric acid (UA) is a relevant risk factor for arteriolosclerosis and recent studies have demonstrated the positive relationship between UA concentrations and the severity of leukoaraiosis. However, the association between lacunar infarcts (LI) and UA levels has seldom been reported in the literature. The aim of our study was to assess whether serum UA levels may be related to the presence of LI. We recruited 242 patients (113 males and 129 females, aged 82.83 ± 6.49 years) from our Geriatric Department for whom CAT scans (CT) were available. Clinical and laboratory data was collected. Patients CT images were examined to identify the presence, the size, the number, and the location of LI. LI without neurological symptoms were considered silent LI. Serum UA levels were found to be positively associated with the presence (p = 0.0001), the number (p = 0.001), the size (p = 0.001), and the location of LI in the basal ganglia (p = 0.0038), the deep white matter (DWM) (p

Background: Lacunar infarcts located in centrum-semiovale and lobar regions were more frequent in Caucasians with intracerebral hemorrhage related to cerebral amyloid angiopathy (CAA-ICH) while deep-seated lacunes in ICH related to hypertension (HTN-ICH), but these associations have never been validated in Asian patients. In the present study, we evaluated whether lobar lacunes were associated with core CAA markers such as lobar microbleeds (CMB) and higher amyloid load on 11 C-Pittsburgh Compund B (PiB) PET in an Asian ICH population. Methods: One hundred and ten patients of primary ICH who received MRI scans were classified as CAA-ICH or HTN-ICH according with the presence of strictly lobar or strictly deep bleeds (both ICH and CMBs), respectively. Lacunes were evaluated in the supratentorial area and classified as lobar (when located in CSO, frontal, parietal, insular/subinsular, temporal, and occipital lobes) or deep (when located in thalamus, basal ganglion, internal and external capsule) based on the location. A subgroup of 36 patients also underwent PiB-PET and global standardized uptake value ratio (SUVR) were calculated. Results: There were 24 CAA-ICH (mean age 70.9 ± 13.9) and 86 HTN-ICH (mean age 59.3 ± 13.0). Lobar lacunes were more frequent in CAA-ICH than HTN-ICH (29.2 vs 11.6%, p=0.036). In univariate analysis, lobar lacunes were significantly related to lobar CMB (pr =0.34, p=0.04). Conclusion: Lobar lacunes were more frequent in Asian patients with CAA-related strictly lobar hemorrhages. Their independent association with lobar CMB and brain amyloid deposition suggests a strong relationship with CAA even in an Asian cohort with overall higher hypertensive load.

Thalamic infarcts, accounting for approximately 14% of lacunar infarcts, exhibit varied clinical manifestations due to complex anatomy of nuclei and varying blood supply. Pure and combined types of thalamic infarctions have been summarized in some paper, but information of cerebral angiography was not mentioned. Here we report a rare case of combined tuberothalamic and paramedian artery occlusion presenting with ipsilateral ptosis and contralateral ataxic hemiparesis.

Background and aims Enlarged basal ganglia perivascular spaces (BG-PVS) are a marker of cerebral small vessel disease (SVD). The association between enlarged BG-PVS and atherosclerosis has been explored, but knowledge is limited to extracranial vessels. We aimed to assess whether enlarged BG-PVS correlate with carotid siphon calcifications (CSC), used as a surrogate of intracranial atherosclerosis. Methods Atahualpa residents aged ≥60 years underwent head computed tomography (CT) for assessment of CSC, and brain magnetic resonance imaging (MRI) for evaluation of BG-PVS and other imaging markers of SVD. We evaluated the association between BG-PVS and CSC severity (dependent variable) using regression models adjusted for demographics and cardiovascular risk factors. Results Of 437 candidates, 354 (81%) were included. Grade 1 CSC were observed in 131 (37%), Grade 2 in 99 (28%), Grade 3 in 92 (26%), and Grade 4 in 32 (9%) subjects. MRI showed >10 enlarged BG-PVS in 97 (27%) participants, moderate-to-severe white matter hyperintensities in 81 (23%), lacunar infarcts in 39 (11%), and deep microbleeds in 28 (8%). Fully-adjusted models showed a significant association between enlarged BG-PVS and CSC severity. Individuals with Grade 4 CSC have 3 times de odds of having enlarged BG-PVS than those with Grade 1 CSC. Enlarged BG-PVS were observed in 20% versus 41% of individuals with Grade 1 and Grade 4 CSC, respectively. Conclusions Enlarged BG-PVS often coexist with CSC, suggesting that a common pathogenetic mechanism may explain the occurrence of both conditions.

ibIntroduction/b: Mixed dementia (MixD) refers to a combination of definite Alzheimer's disease (AD) and vascular encephalopathy. The existence of a "pure" type of vascular dementia (VaD) is controversial. There is a need to find magnetic resonance imaging (MRI) characteristics allowing the distinction between VaD and MixD. The present post-mortem 7.0-tesla MRI compares the frequency or severity and the topography of the small cerebrovascular lesions in brains of patients with VaD and with MixD.bMaterial and methods/b: Based on neuropathological criteria, 14 brains were classified as VaD, 24 as MixD and 11 as controls. Three coronal sections of a cerebral hemisphere and a horizontal section of a cerebellar hemisphere underwent T2 and T2* 7.0-tesla MRI examination. The mean values and topographic distribution of white matter changes (WMCs), lacunar infarcts (LIs), cortical microbleeds (CoMBs) and cortical microinfarcts (CoMIs) were determined and compared between the different groups.bResults/b: Compared to the controls, both VaD and MixD brains had significantly more severe WMCs and increased numbers of CoMBs and CoMIs. Lacunar infarcts predominated only in the VaD cases. On mutual comparison of VaD and MixD brains, CoMBs and CoMIs predominated in the frontal lobe and the cerebellum of VaD, while were mainly present in the occipital lobe of MixD. White matter changes predominated in the temporal lobe of MixD cases. Lacunar infarcts were significantly increased in the corona radiata and putamen of VaD patients.bConclusions/b: The present post-mortem MRI study shows clear differences in the distribution and the types of cerebrovascular lesions on high-field MRI, confirming that VaD and MixD are different diseases./i.

Background: Cerebral small vessel disease (SVD) affects small perforating arteries, causing both lacunar infarction (LI) and confluent white matter lesions (WML). Small vessel disease or lacunar infarct is one of the major stroke subgroups. Lacunar syndromes may be divided into two groups: the classic group (pure motor hemiplegia, pure sensory stroke, ataxic hemiparesis, dysarthria-clumsy hand syndrome, sensorimotor stroke) and the miscellaneous group, including all other lacunar syndromes. We have evaluated risk factors, clinical syndromes, topography, and laboratory findings of 101 consecutive patients with symptomatic lacunar infarcts diagnosed by magnetic resonance imaging.Methods: We analyzed 101 patients with clinical lacunar infarct syndrome who were referred to the neurology department of Qa’em hospital, Mashhad in the northeast of Iran. We assessed clinical features, sex, age, risk factors, radiologic findings and laboratory data of these patients.Results: The pure motor hemiparesis (53.5%) constituted the most usual lacunar syndrome. Mean age of the patients was 63.7± 8.5%. Diabetes mellitus was seen in 14 (13.9%) and hypercholesterolemia in 41 (40.6%) of patients. There were significant differences among ataxic-hemiparesis syndrome and hypertriglyceridemia and CVA history. There was a significant difference between miscellaneous syndromes and valve disease history. Also, there was significant correlation between WML and smoking. Thirty percent of the lesions were detected by CT scan.Conclusion: Sixty percent of the cases were associated with white matter signal changes. Diabetes mellitus were found in 14% of patients. Hypertriglyceridemia, CVA history and valve disease history were associated with some subgroups, but more investigations should be performed for precise assessment of other risk factors.

MRI evidence of white matter hyperintensity (WMH), lacunar infarcts, and cerebral microbleeds characterizes cerebral small vessel disease (SVD).1 These microangiopathic imaging markers occur with high prevalence in Fabry disease (FD), an X-linked lysosomal storage disorder caused by mutations in the α-galactosidase A (GLA) gene leading to the accumulation of globotriaosylceramide in different cellular compartments, especially the lysosome.2 However, the underlying mechanisms for cerebrovascular damage in SVD and FD may fundamentally differ as prior studies have demonstrated an increase of cerebral blood flow (CBF) in FD,3,4 whereas patients with sporadic SVD typically have reduced CBF.5

CLIPPERS (chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids) is a recently described chronic inflammatory disorder involving the brainstem with characteristic imaging findings. Since it was originally described in 2002, only a handful of cases have been reported in the literature. We describe two additional cases of CLIPPERS with characteristic clinical and radiological findings. Besides the previously described MR findings, one of the cases also demonstrated multiple basal ganglia lacunar infarcts, a finding which has not been previously reported. We hypothesize that the lacunar infarcts are caused by this chronic infiltrative perivascular disease process.

Objective: This study evaluated the efficacy of combined therapy with probucol and cilostazol on endothelial function in silent lacunar cerebral infarcts (SLCI) and mild hypercholesterolemia. Subjects and Methods: Flow-mediated vasodilatation (FMD) and nitroglycerin-induced vasodilatation (NMD) were measured before and after 4 weeks of combined therapy with probucol (500 mg/day) and cilostazol (200 mg/day) in 34 patients with a mean age of 72 ± 7 years (range 57-80 years) with SLCI, mild hypercholesterolemia (low-density lipoprotein cholesterol >100 mg/dl) and impaired endothelial function (FMD Results: Although the baseline FMD was not different between the two treatment arms (2.7 ± 1.5 vs. 2.6 ± 1.5%, n.s.), the posttreatment FMD was significantly improved in the PC group (from 2.7 ± 1.5 to 3.5 ± 1.7%, p < 0.05) but not in the A group (from 2.6 ± 1.5 to 2.9 ± 1.4%, n.s.). No differences were observed between baseline and posttreatment NMD in either group. The effects of treatments on lipid profiles were more profound in the PC group. Conclusion: Combined treatment with probucol and cilostazol resulted in subacute improvement in FMD/endothelial function in patients with SLCI with mild hypercholesterolemia. This combination therapy has the potential to reduce the risk of cardiovascular events via improvements in endothelial function and lipid profiles.