Search

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

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 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.

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.

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.

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.

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.

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.

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.

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

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.

Background and Purpose— Asymptomatic lacunar infarcts, white matter lesions, cerebral microbleeds, and enlarged perivascular spaces are MRI markers of cerebral small vessel disease (cSVD). Higher blood pressure (BP) levels are associated with the presence of these markers separately, but the association with the total burden of cSVD on brain MRI, expressed by the simultaneous presence of multiple markers of cSVD (a compound score), has not been investigated. Methods— We performed 24-hour ambulatory BP monitoring in 122 patients with first-ever lacunar stroke. On brain MRI, we scored the presence of each marker of cSVD. One point was awarded for the presence of each marker, producing a score between 0 and 4. Associations with BP levels were tested with ordinal regression analyses. Results— Eighteen (15%) patients had no markers of cSVD, and 6 (5%) patients had 4 markers. Most patients (45; 37%) had 2 different markers. After correction for age and sex, higher 24-hour, day, and night systolic (24-hour odds ratio, 1.25; 95% confidence interval, 1.02–1.52 per 10 mm Hg) and diastolic (24-hour odds ratio, 1.32; 95% confidence interval, 1.12–1.56 per 5 mm Hg) BP were all significantly associated with an increasing total burden of cSVD. Conclusions— We found a positive association of ambulatory BP levels with total burden of cSVD on brain MRI. With increasing BP levels, there is a piling up of damage in the brain. We suggest that further cSVD studies also consider viewing the total burden in addition to each of the MRI markers separately.

Objective— Basilar arterial (BA) dolichoectasia is associated with cerebral small-vessel disease and stroke. However, the association between moderate dilation of the BA and cerebral small-vessel disease or subsequent cardiovascular events remains unclear. This study aims to clarify the factors related to BA diameter and to clarify whether the BA diameter is an independent predictor of cardiovascular events. Approach and Results— The study subjects comprised 493 outpatients with atherosclerotic risk factors. BA diameter, lacunar infarct, severity of deep white matter hyperintensities, and intracranial steno-occlusive lesions were assessed with MRI and magnetic resonance angiography. Then, we prospectively evaluated the association between BA diameter and cardiovascular events. The BA diameter ranged from 1.1 to 5.2 mm, and only 0.8% of the patients had dolichoectasia. Male sex, the presence of lacunar infarcts, the severity of deep white matter hyperintensities, the fetal-type variation of the circle of Willis, and intracranial steno-occlusive lesions were independently associated with BA diameter. In the mean follow-up of 6.0 years, 91 patients developed cardiovascular events. BA diameter was independently associated with total cardiovascular events after adjusting for age, sex, and conventional risk factors (hazard ratio, 1.55 per 1 mm increase in BA diameter; P =0.009). Conclusions— Increased BA diameter within the normal range is related to both large-vessel disease and cerebral small-vessel disease, and it could be a new predictor of cardiovascular events.

Background and Purpose— Lacunar stroke (LS) and intracerebral hemorrhage (ICH) are 2 diverse manifestations of small vessel disease. What predisposes some patients to ischemic stroke and others to hemorrhage is not well understood. Methods— We performed a nested case–control study within the FHS (Framingham Heart Study) comparing people with incident ICH and lacunar ischemic stroke, to age- and sex-matched controls for baseline prevalence and levels of cardiovascular risk factors. Results— We identified 118 LS (mean age 74 years, 51% male) and 108 ICH (75 years, 46% male) events. Hypertension, diabetes mellitus, smoking, and obesity were strongly associated with LS. Hypertension, but not diabetes mellitus, smoking, or cholesterol levels increased the odds of ICH. Contrary to LS, ICH cases had lower body mass index (BMI) than their controls (26 versus 27); BMI Conclusions— LS and ICH share hypertension, but not diabetes mellitus, as a common risk factor. ICH cases had lower BMI compared with not only LS but their controls as well; this finding is unexplained and merits further exploration.

Lacunar (small deep) and small centrum ovale infarcts (LACIs and SCOIs, respectively) are both small subcortical infarcts with the same appearance on computed tomography (CT), but they are located in

Objective Cerebrovascular lesions (CVLs) are known to play important roles in the pathophysiology underlying Alzheimer's disease (AD), especially in elderly AD cases. The present study was conducted to elucidate the relationship between the CVLs and vascular risk factors (VRFs) in elderly Japanese patients with AD. Subjects and methods The CVLs such as lacunar infarcts, old microbleeds (OMBs), white matter lesions (WMLs), and occlusive vascular lesions on MRI were analyzed in relation to the risk factors in 120 Japanese patients with probable AD. Their mean age was 75.6 years. The subjects were divided into two age groups: young-old group (YOG) consisting of 55 cases being younger than 75 years and old-old group (OOG) consisting of 65 cases being 75 years or older. Results In overall analysis, 10 cases (8.3%) showed brain atrophy without CVLs on MRI, 46 cases (38.3%) showed WMLs in addition to the brain atrophy, 61 cases (50.8%) showed lacunar lesions, and 3 cases (2.5%) were diagnosed as having a superficial siderosis. Lacunar infarcts and OMBs were more frequently observed in OOG than in YOG, and were also more frequently observed in those with 2 or more VRFs than those with less than 2 VRFs (p Conclusion The CVLs including lacunes, WMLs, and OMBs were present more than 90% of elderly Japanese patients with AD. As the severity of CVLs was associated with VRFs and age, VRFs may modify clinical presentation of elderly AD patients.

Background and Purpose— Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) phenotype is highly variable, and, although the full clinical–neuroimaging picture may be suggestive of the disease, no characteristic is pathognomonic. Thus, a genetic test remains the diagnostic gold standard, but because it is costly and time-consuming, a pregenetic screening appears desirable. We aimed at developing the CADASIL scale, a screening tool to be applied in the clinical setting. Methods— A preliminary scale was created assigning weighted scores to common disease features based on their frequencies obtained in a pooled analysis of selected international CADASIL series. The accuracy of the scale versus the genetic diagnosis was tested with receiver operating characteristic analysis after the application of this scale to 61 CADASIL and 54 NOTCH3 -negative patients (no pathogenic mutation on exons 2–23 of the NOTCH3 gene). To improve the scale accuracy, we then developed an ad hoc optimization algorithm to detect the definitive scale. A third group of 39 patients affected by sporadic small-vessel disease was finally included in the algorithm to evaluate the stability of the scale. Results— The cutoff score of the definitive CADASIL scale had a sensitivity of 96.7% and a specificity of 74.2%. This scale was robust to contamination of patients with sporadic small-vessel disease. Conclusions— The CADASIL scale is a simple and sufficiently accurate screening tool to select patients with a high probability to be affected by the disease and therefore to be subjected to the genetic testing.

Background and Purpose— Definitions for chronic lacunar infarcts vary. Recent retrospective studies suggest that many acute lacunar strokes do not develop a cavitated appearance. We determined the characteristics of acute lacunar infarcts on follow-up MRI in consecutive patients participating in prospective research studies. Methods— Patients with acute lacunar infarction on diffusion-weighted imaging were selected from 3 prospective cohort studies of minor stroke imaged within Results— Probable or definite cavitation on any sequence was more common at 90 days compared with 30 days ( P ≤0.001 for all sequences). At 90 days, evidence of cavitation was seen on at least 1 sequence in 33 of 34 patients (97%). The T1-weighted sequence was most sensitive to the presence of cavitation (94% at 90 days). By contrast, the fluid-attenuated inversion recovery sequence frequently failed to show evidence of cavitation in the brain stem or thalamus (only 10 of 18 [56%] showed cavitation). Conclusions— MRI scanning at 90 days with T1-weighted imaging reveals evidence of cavitation in nearly all cases of acute lacunar infarction. By contrast, reliance on fluid-attenuated inversion recovery alone will miss many cavitated lesions in the thalamus and brain stem. These factors should be taken into account in the development of standardized criteria for lacunar infarction on MRI.

Objective: We aimed to analyze lesion patterns of lacunae-sized infarctions in the perforating arterial territory in terms of shape and to determine whether the particular pattern of conglomerated beads shape affected early neurologic deterioration. Methods: We consecutively included acute ischemic stroke patients with confirmed lacunae-sized acute ischemic infarcts in the penetrating arterial territories on diffusion-weighted MRI. Based on diffusion-weighted MRI, the shape of ischemic infarcts was divided into oval or conglomerated beads shape. Demographics, risk factors, NIH Stroke Scale (NIHSS) score at admission and discharge, and stroke mechanisms were analyzed. Early neurologic deterioration was defined as any increase of NIHSS score at the time of discharge. Results: Among 105 patients included, the conglomerated beads shape of infarcts was observed in 34 (32.4%) patients and the oval shape in 71 (67.6%) patients. The baseline characteristics were not different between the 2 groups. However, the maximal diameter of the lesion was significantly larger in the conglomerated beads shape group (12.8 ± 3.3 mm vs 10.8 ± 3.8 mm, p = 0.009). Early neurologic deterioration was also more commonly observed in the conglomerated beads shape group than in the oval shape group (20.6% vs 4.2%, p = 0.012). Multiple logistic regression analysis showed that the conglomerated beads shape was significantly associated with early neurologic deterioration (odds ratio 6.83, 95% confidence interval 1.53–30.55, p = 0.012). Conclusions: In 32.4% of all the lacunae-sized infarcts in the perforating artery territory, the conglomerated beads shape was observed. This shape was significantly associated with early neurologic deterioration.

Summary‘Cerebral small vessel disease’ is common in older adults and is an important cause of morbidity, functional impairment and cognitive decline. Small vessel disease is a collective term used to describe a number of underlying pathological processes and neuroimaging findings, such as lacunar infarcts, white matter lesions and microhaemorrhages.With readily available neuroimaging, diagnostic accuracy has improved; however, the management of small vessel disease and prevention of cognitive decline remains uncertain. Treatment of conventional vascular risk factors may be appropriate, but future research is required to provide definitive answers. We have conducted a comprehensive literature review of cerebral small vessel disease in older adults. This highlights the clinical sequelae and underlying pathological processes, whilst discussing novel diagnostic neuroimaging and therapeutic strategies.

Spontaneous non traumatic intracerebral haemorrhage (ICH) is usually caused by many different interacting factors, such as the use of alcohol or fibrinolitic drugs, congenital aneurysm, brain tumors, and blood dyscrasia. Age and hypertension-related small vessel diseases, and cerebral amyloid angiopathy are the most common forms of vascular damage which can lead to ICH. Furthermore, a group of inherited cerebral small vessel diseases linked to ICH have been reported recently and the number of these forms is increasing. The presence of leukoaraiosis, lacunar infarcts and microbleeds has been suggested to indicate a higher risk for cerebral hemorrhage. In recent years, MRI and neuroimaging techniques contributed to the understanding and the diagnosis of this disease.

Background and Purpose— On brain imaging, lacunes, or cerebrospinal fluid–containing cavities, are common and are often counted in epidemiological studies as old lacunar infarcts. The proportion of symptomatic lacunar infarcts that progress to lacunes is unknown. Noncavitating lacunar infarcts may continue to resemble white matter lesions. Methods— We identified patients with acute lacunar stroke, with or without an acute lacunar infarct on computed tomography or MRI, who had follow-up imaging. A neuroradiologist classified lacunar infarcts progressing to definite or possible cavities on follow-up imaging. We tested associations between cavitation and patient-related, stroke-related, and imaging-related features, including other features of small vessel disease. Results— Among 90 patients (mean age 67 years), any cavitation was present on follow-up imaging in 25 (28%), and definite cavitation in 18 (20%). Definite cavitation was associated with increasing time to follow-up imaging (median 228 days, range 54 to 1722, versus no cavitation 72 days, range 6 to 1440; P =0.0003) and deep cerebral atrophy ( P =0.03) but not with age, stroke severity, larger initial infarct size, or other features of small vessel disease. Hypertension and diabetes were negatively associated with cavitation ( P =0.01 and 0.02, respectively). Conclusions— Definite cavitation occurs in one fifth of symptomatic lacunar ischemic strokes, implying that most continue to resemble white matter lesions. Epidemiology and pathophysiology studies of lacunar stroke, which have only counted lacunes as lacunar infarcts, may have substantially underestimated by as much as 5 times the true burden of lacunar stroke disease.

Background: Cardiovascular risk factors, clinical features and early outcome of first-ever cerebral lacunar infarcts from 1986 to 2004, using the Sagrat Cor Hospital of Barcelona Stroke Registry, were assessed and compared with data from patients with nonlacunar infarction. Methods: The study population consisted of 566 patients with lacunar infarct and 1,516 patients with nonlacunar infarct. Secular trends for the periods 1986–1992, 1993–1998 and 1999–2004 were analyzed. Results: Age and the percentage of very old patients (≧85 years old) increased significantly (p < 0.001) throughout the time period. There was a significant decrease in the percentage of patients with hypertension, but the percentage of patients with chronic obstructive pulmonary disease increased. The use of brain magnetic resonance imaging (MRI) also increased significantly. The median length of hospital stay decreased significantly. Conclusions: Significant changes over a 19-year period included an increase in the patients’ age, frequency of very old patients (≧85 years old) and use of MRI studies, whereas the frequency of hypertension and length of hospital stay decreased.

The past 25 years have witnessed a dramatic rise and fall in clinical research investigating lesion localization in poststroke depression patients. Early studies focused on basic lesion characteristics, such as left versus right hemisphere and anterior versus posterior location, that would dominate studies in this field for the next 15 years. While results were inconsistent, some studies suggested that the left hemisphere and more anterior lesions were associated with increased prevalence and severity of depression. Recent studies have suggested lesion preference in components of the basal ganglia and frontal–subcortical circuitry and have proposed a combined effect of large stroke lesions and other lesions, such as white matter hyperintensities and lacunar infarcts. The effect of lesion location on poststroke depression requires further clarification.

Background: Cerebral small vessel diseases, including silent lacunar infarcts, white matter hyperintensities, and microbleeds, pose a risk for cerebrovascular disease, cognitive impairment, and the geriatric syndrome via effects on arterial stiffness. However, the vascular, physiological, and metabolic roles of arterial stiffness in cerebral small vessel diseases remain unclear. Summary: Arterial stiffness can be assessed using various indicators such as the ankle-brachial index, pulse wave velocity, cardio-ankle vascular index, and augmentation index. Arterial stiffness is independently associated with all components of cerebral small vessel disease including silent lacunar infarcts, white matter hyperintensities, and microbleeds, although there are some methodological differences between the various surrogate markers. Evidence of arterial stiffness indicates microvessel arteriosclerosis presenting with vascular endothelial dysfunction. Further, vascular narrowing due to atherosclerosis and vascular stiffness due to lipohyalinosis can accelerate the pulse waves. This hemodynamic stress, pulsatile pressure, or blood pressure variability can cause a ‘tsunami effect' towards the cerebral parenchyma and lead to cerebral small vessel disease. Previous studies have shown that silent lacunar infarcts and white matter hyperintensities are strongly associated with arterial stiffness. However, the association between microbleeds and arterial stiffness remains controversial, as there are two vessel mechanisms related to microbleeds: cerebral amyloid angiopathy and hypertensive small vessel disease. Key Messages: Cerebral small vessel disease with associated arterial stiffness is a risk factor for silent cerebral lesions, stroke, and cognitive impairment. Improvement of the living environment, management of risk factors, and innovation and development of novel drugs that improve arterial stiffness may suppress the progression of cerebral small vessel disease, and may reduce the risk for stroke and dementia.

Background: Family and twin studies suggest predisposing genetic factors in stroke. Lacunar infarcts represent a homogeneous phenotype, which is a prerequisite for genetic analyses. Applying an affected sib -pair analysis, we prospectively assessed the prevalence of microangiopathic brain lesions (MBL) and associated risk factors among siblings of patients with lacunar stroke. Methods: Index patients fulfilled clinical criteria of a lacunar stroke in combination with a corresponding MBL on CT or MRI. Siblings were characterized as affected if MBL demonstrated on MRI. The prevalence of MBL was compared with population prevalence data extracted from other studies. Results: From 784 patients screened, 81 index patients with lacunar stroke and 97 siblings were recruited, of which 42% were identified as affected. Compared with data from unselected historical controls and stratified by age groups, prevalence was between 2 and 5 times higher. Conclusions: Our results indicate that genetic stroke studies are feasible even in subtypes of ischemic stroke. The high prevalence of MBL among siblings of patients with lacunar infarct might suggest a familial aggregation. However, due to the small sample size these results need to be interpreted with caution and require confirmation by planned genetic analyses.

Right-to-left shunt (RLS) is associated with cryptogenic stroke and migraine. Herein we investigated the relationship between RLS and silent lacunar infarcts in patients with migraine. A total of 263 patients with migraine who met eligibility criteria were enrolled from January 2010 to December 2011, among which 127 subjects fell into RLS group. Baseline demographics were comparable between RLS and non-RLS groups (P>0.05). The incidence of silent lacunar infarcts in RLS group was not significantly different from that of the non-RLS group (25.2% versus 21.3%,P>0.05). Furthermore, we found that the incidence of silent lacunar infarcts in permanent and latent RLS subgroups was comparable with non-shunt RLS subgroup (28.6% versus 24% versus 21.3%,P>0.05). Similarly, the incidence of silent lacunar infarcts in the non-RLS group, mild-shunt group, and large-shunt group was also comparable (21.3% versus 23.8% versus 29.3%,P>0.05). In addition, RLS did not increase the incidence of silent lacunar infarcts in migraine patients with elder age (P>0.05). In conclusion, RLS does not increase the incidence of silent lacunar infarcts in patients with migraine. Further prospective studies are warranted to validate this finding.

Lacunar infarcts and "hypertensive" primary intracerebral hemorrhages, collectively often referred to as hypertensive small vessel strokes, constitute about one third of all strokes. However, despite their public health importance, their etiopathogenesis remains ill-understood. Like all strokes, they are a heterogeneous entity, but the autopsy pathology evidence suggests that the majority are caused by a limited number of cerebral small vessel lesions. Small vessel atherosclerosis is causally implicated in a proportion of lacunar infarcts, although modern concepts of atherosclerotic plaque biology and natural history have yet to be applied to small cerebral vessels. A lesion characterized in its acute form by fibrinoid necrosis appears to be important in causing both lacunar infarcts and primary intracerebral bleeds. Advances in molecular genetics may prove instrumental in understanding the cause of this lesion and therefore in designing its targeted prevention.

Introduction: Microhemorrhages seen on gradient-echo magnetic resonance imaging are thought to be a manifestation of small-vessel disease. It was the aim of our study to evaluate the prevalence of microhemorrhage for patients presenting with acute lacunar infarction. Methods: We obtained gradient-echo and diffusion-weighted magnetic resonance imaging as part of the acute stroke workup in 46 patients presenting with lacunar infarction. Results: Gradient-echo magnetic resonance imaging was abnormal in 24 of 46 (52%) patients. Microhemorrhage was seen in 21 patients (46%), 2 patients had multiple microhemorrhages and a frank hemorrhage, and 3 patients had frank hemorrhage in the absence of microhemorrhage. Prior symptomatic stroke was the only significant risk factor for the presence of microhemorrhages. Conclusion: Microhemorrhages are present in approximately half of patients with lacunar infarcts and appear to be a marker of severity of small-vessel disease.

Vascular dementia and vascular cognitive impairment have attracted more attention recently due to their association with increased risk of death and institutionalization. The purpose of the present study was to detect and identify the characteristics of cognitive impairments during the early stage of lacunar stroke. The subjects consisted of 23 consecutive first-ever acute lacunar infarction patients who were admitted to the Department of Neurology, Kaohsiung Municipal Hsiao-Kang Hospital, Taiwan, from November 2001 to October 2002. The National Institutes of Health Stroke Scale and Cognitive Abilities Screening Instrument (CASI) were used to evaluate stroke severity and cognitive function, and assessments were performed by a neurologist and psychologist, within 10 days of stroke onset. Of the 23 patients, 21 (91.3%) had CASI scores below their respective cutoff values and all patients had cognitive impairment in at least one cognitive domain in CASI. There were no significant correlations between CASI abnormality (below the cutoff value) and patient age, education, or the interval from stroke onset. Recent memory impairment was the most often impaired cognitive domain on CASI (19 patients, 82.6%). There were significant correlations between recent memory and “attention or concentration” (correlation coefficient, 0.52; p < 0.05), and “abstraction and judgment” (correlation coefficient, 0.44; p < 0.05). The correlations between recent memory and other domains were not significant. It was concluded that cognitive impairment after acute lacunar infarct is quite common and recent memory is the most often impaired cognitive domain. This may have been caused by the location of the specific lesion as well as by the impairment in “attention or concentration” or “abstraction and judgment”.

Background: Twenty-four-hour blood pressure (BP) readings have been found to correlate with hypertensive target organ damage. Lacunar infarcts (LI) and white matter lesions (WML) probably represent manifestations of cerebral hypertensive target organ damage. This study was conducted to better delineate the relationships between 24-hour BP measurements, LI/WML and small vessel disease cognitive impairment/vascular dementia (CI/VD). Methods: Two hundred patients with first-time symptomatic LI were examined with 24-hour BP monitoring. The degree of nocturnal BP dip, (daytime BP – nighttime BP)/daytime BP, was categorized into three groups: dippers (>0.1), nondippers (0–0.1) and reverse dippers (Results: The breakdown of patients was: 50% nondippers, 27.5% reverse dippers and 22.5% dippers. Forty-one patients (20.5%) were found to have CI and dementia. Male sex (OR 3.35; 95% CI 1.20–9.34), advanced PVH (OR 14.42; 95% CI 5.62–36.98) and absence of a dipping status (nondipper: OR 12.62; 95% CI 1.37–115.95; reverse dipper: OR 11.95; 95% CI 1.27–112.11) were independently associated with CIVD after multivariate analysis. High nighttime systolic BP (OR 3.93; 95% CI 1.38–11.17), high daytime (OR 2.06; 95% CI 1.03–4.04) and nighttime diastolic BP (OR 2.48; 95% CI 1.13–5.45) and absence of a dipping status (nondipper: OR 2.7; 95% CI 1.03–7.05; reverse dipper: OR 3.78; 95% CI 1.38–10.34) were significantly associated with PVH. Conclusions: High prevalence of a nondipping status was found in the LI cohort. A nondipping status appears to be directly associated with CIVD independent of PVH. This study indicates the need for further studies to investigate whether or not controlling nighttime BP will help reduce the risk for CI/VD development.

Stroke secondary to polycythemia rubra vera (PRV) is very uncommon. A 55 years old man presented to us with ischaemic stroke, imaging revealed one recent and multiple previous Lacunar infarcts. Evaluation for underlying cause proved him as a case of PRV. Effective treatment of PRV can prevent the further recurrence of Ischaemic stroke DOI: http://dx.doi.org/10.3329/akmmcj.v4i1.13686 AKMMC J 2013: 4(1): 45-47

Microbleeds (MBs) detected by gradient-echo T2*-weighted MRI (GRE-T2*),white matter changes and lacunar infarcts may be regarded as manifestations of microangiopathy. The establishment of a quantitative relationship among them would further strengthen this hypothesis. We aimed to investigate the frequency and the number of MBs in patients hospitalized with lacunar infarcts and their quantitative relationship with the severity of white matter changes (WMC) and the number of old lacunar infarcts. We performed a hospital-based survey of patients with acute lacunar infarct. Eighty-two consecutive Chinese patients with acute lacunar infarcts on diffusion-weighted imaging were recruited in 2002. The number of MBs, number of old lacunar infarcts on T2-weighted imaging and the severity of WMC on MRI on admission were recorded. MBs were detected in 22 (27%) patients. The number of MBs ranged from 1 to 42 (mean 6.59, median 3). Advancing age and previous transient ischemic attacks or cerebrovascular accidents (TIA/CVA) were more common in patients with MBs than those without. There were significant correlations among the number of MBs, extent of WMC and number of lacunar infarcts: lacunar infarcts and MBs (r = 0.297, p = 0.007); lacunar infarct and WMC (r = 0.331, p = 0.002); WMC and MBs (r = 0.522, p < 0.0001). In conclusion, linear associations exist among MBs, WMC and lacunar infarcts. Our results suggest that all three may have a shared pathogenesis such as advanced microangiopathy.