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Previous studies have shown the potential interactions between cerebrovascular diseases and microalbuminuria. However, the relationship between urine microalbumin and acute lacunar infarction caused by cerebral small vessel disease (CSVD) remains unknown.The clinical data of 148 patients with acute lacunar infarction admitted to the Department of Neurology, Shengjing Hospital of China Medical University between April 2016 and April 2017 were analyzed. They were divided into either a CSVD group (n = 70) or a cerebral large vessel disease (CLVD) group (n = 78) according to their carotid artery B-mode ultrasonography and head magnetic resonance angiography (MRA) findings. The concentration of urinary microalbumin in both groups was determined. Statistic analysis was conducted using SAS 9.1 software (North Carolina state university, USA). A Logistic regression analysis was used to determine the independent risk factors for acute lacunar infarction caused by CSVD.The concentration of urine microalbumin in the CSVD group (23 ± 12 mg/L) was significantly lower than that in the CLVD group (29 ± 15 mg/L) (p 0. 01). However, there was an increasing trend for the proportion of patients with urine microalbumin concentration 10- 30 mg/L (34.3%) in the CSVD group compared with the CLVD group (19.2%). Logistic regression analysis showed that microalbuminuria (10- 30 mg/L) was independently associated with acute lacunar infarction caused by CSVD (OR = 3.582; 95% CI 1.347～6.274; p 0.01).These findings demonstrate that in patients with acute lacunar infarction, slightly increased microalbuminuria seems to be a potential clinical marker for CSVD. The presence of microalbuminuria early may help to differentiate CSVD from stroke subtypes.

Background and Purpose— We investigated the frequency and pattern of blood-brain barrier, as well as blood-retina barrier, impairment in acute lacunar infarction as demonstrated by hyperintense acute reperfusion marker and gadolinium leakage in ocular structures (GLOS), respectively, on fluid-attenuated inversion recovery images. Methods— Acute lacunar infarction patients who underwent repeated magnetic resonance imaging after intravenous contrast agent administration were identified and the presence of GLOS in the anterior chamber and vitreous body and hyperintense acute reperfusion marker noted on fluid-attenuated inversion recovery. Results— Overall, 24 acute lacunar infarction patients (median age 64.5 years; interquartile range, 54–78 years) were included. On contrast-enhanced fluid-attenuated inversion recovery, GLOS was observed in 11 (45.8%) patients: in 4 (16.7%) in the anterior chamber only and in 7 (29.2%) in the anterior chamber and vitreous body. In all patients, GLOS was bilateral and symmetrical. In patients with GLOS in the anterior chamber only, the time between initial and follow-up magnetic resonance imaging was significantly shorter (7.5 [interquartile range, 4.25–11.5] hours) compared with patients with GLOS in the anterior chamber and vitreous body (28 [interquartile range, 10–43] hours; P =0.047). Hyperintense acute reperfusion marker could not be demonstrated in any of the patients. Conclusions— In acute lacunar infarction patients, unlike hyperintense acute reperfusion marker, GLOS is a frequent finding and shows a similar temporal evolution like in larger ischemic stroke.

Usefulness of intravenous thrombolysis in patients with acute lacunar cerebral infarction is questionable. The aim of this study was to evaluate the efficacy and safety of intravenous thrombolysis in patients with lacunar infarction in comparison with patients with nonlacunar infarction as well as with patients with lacunar infarction who were not treated with intravenous thrombolysis.In the first part of the study, among patients with acute ischemic stroke treated with intravenous thrombolysis, characteristics and outcomes of 46 patients with lacunar and 221 patients with nonlacunar infarction were compared. In the second part, 46 patients with lacunar infarction treated with intravenous thrombolysis were compared with 45 lacunar infarction patients who were not treated with intravenous thrombolysis.Patients with lacunar infarction had a lower National Institutes of Health Stroke Scale score (9.2 versus 13.9, P.001), a greater Alberta Stroke Program Early computed tomography (CT) score (9.7 versus 9.2, P = .002), a lower prevalence of atrial fibrillation (6.5% versus 41.2%, P.001), and significantly more frequently an excellent outcome after 3 months (76.1% versus 36.2%, P.001) compared with patients with nonlacunar infarction. Among patients with lacunar infarction, an excellent outcome at discharge was significantly more frequent in the intravenous thrombolysis group (41.3% versus 15.6%, P = .01), and the length of hospitalization was significantly shorter (9.5 days versus 14.3 days, P = .002). There was no hemorrhagic transformation among patients with lacunar infarction treated with intravenous thrombolysis.Intravenous thrombolysis has proven to be effective and safe in patients with lacunar infarction and should always be applied if there are no absolute contraindications.

Background: It has been reported that some patients with lacunar infarction have transient ischemic attacks (TIAs) before stroke. This study was aimed at evaluating the factors and prognostic value related to TIAs preceding acute lacunar stroke. Methods: A total of 1,424 patients were admitted to the hospital for first-ever ischemic stroke. Of which 314 patients with acute lacunar infarction were enrolled for this study. The patients were divided into 2 groups based on the occurrence of TIAs before stroke. Results: Fifty-eight patients (18.5%) had a history of preceding TIAs. The interval between TIA and stroke was less than 24 h in most patients (87.9%). Diabetes mellitus was more often found in patients with TIAs than in those without TIAs (48.3 vs. 28.9%, p = 0.004). Initial National Institute of Health Stroke Scale scores showed no significant difference between the 2 groups (median 2 vs. 3, p = 0.067). However, patients with preceding TIAs had a more favorable outcome (modified Rankin scale 0-1) than those without TIA at 3 months after stroke (79.6 vs. 63.2%, p = 0.021). Conclusion: Lacunar TIA may occur due to small perforating microatheromatous arteries caused by diabetes. This study suggests that ischemic tolerance may play a role in patients with preceding TIAs before lacunar infarct, allowing better recovery from a subsequent ischemic stroke.

The aim of this study was to determine whether pulse wave velocity (PWV), a marker of vascular endothelial impairment and arteriosclerosis, predicts future ischemic stroke in patients who developed acute lacunar infarction. Patients with a first-ever ischemic stroke due to acute lacunar infarction were enrolled in this study. An oscillometric device (Form PWV/ABI; Omron Colin, Tokyo, Japan) was used to measure brachial-ankle PWV 1 week after stroke onset. Patients were followed for at least 5 years. The main end point of the study was recurrent ischemic stroke. Event-free survival was analyzed using Kaplan-Meier plots and log-rank tests. The risk of recurrent ischemic stroke was estimated using the Cox proportional-hazards model. Of the 156 patients (61% male, mean age: 69.2±11.3 years) assessed in this study, 29 developed recurrent ischemic stroke. The median brachial-ankle PWV value was 20.4 m s

Background/Aims: The mechanisms underlying neurological deterioration in patients with acute lacunar infarction in the lenticulostriate artery (LSA) territory are currently unclear. We aimed to identify predictors for progressive neurological deficits using diffusion-weighted imaging (DWI). Methods: We studied 40 consecutive patients who were classified into two groups based on their NIHSS scores: progressive infarction (PI) and non-progressive infarction (NPI). We calculated the size of DWI abnormalities and evaluated clinical characteristics on admission for both groups. Results: 19 patients (47.5%) exhibited neurological deterioration. Time from onset to MRI was 8.2 ± 6.7 h for all patients. DWI area was significantly larger in the PI relative to the NPI group (1.1 ± 0.5 cm2 for PI vs. 0.7 ± 0.3 cm2 for NPI; p = 0.002), although patients’ NIHSS scores at admission were not significantly different between both groups. The optimal cut-off value of infarct area between PI and NPI was 0.98 cm2. Multivariate analysis revealed that an infarct area on DWI ≧0.98 cm2 (odds ratio 10.57; 95% confidence interval 2.24–68.32; p = 0.006) was a significant independent predictor of PI. Conclusions: A large infarct area on initial DWI was an independent predictor of neurological deterioration in patients with acute lacunar infarctions in the LSA territory.

Background: White matter hyperintensities (WMH) predict incident strokes and new lacunes; moreover, WMH may also affect infarct locations. Our aim in this study was to examine the spatial relationship between WMH and acute lacunar infarction. Methods: Five hundred and ninety patients with acute lacunar infarction in supratentorial region were included. Four situations between infarction and WMH were assessed by axial and coronal MRI: no contact (Grade 0), contact without overlap (Grade Ia), partial overlap (Grade Ib), and complete overlap (Grade II) with preexisting WMH. Furthermore, we defined infarctions in Grades Ia and Ib as edge-localized infarctions and investigated their predictors and short-term outcome. Results: 47.9% (283) of the infarctions were edge-localized infarctions (Grade Ia = 27.6% and Grade Ib = 20.3%), 51.5% (304) were Grade 0, only 0.5% (3) were Grade II. Patients with edge-localized infarction had larger infarct size, more severe WMH, higher National Institutes of Health Stroke Scale (NIHSS) and lower Barthel index (BI) score at admission than those with non-edge-localized infarction. They also had lower BI score at discharge. Infarction in subcortical white matter, diffusion-weighted imaging infarct size, periventricular WMH and deep WMH were predictors for edge-localized infarction. Conclusions: Half of lacunar infarctions were located at the edge of WMH. Both periventricular WMH and deep WMH were predictors for edge-localized infarction.

The involvement of matrix metalloproteinases (MMPs) in ischemic-stroke-induced inflammatory response has recently been suggested; however, the relationship between MMPs and stroke progression has not been evaluated. We investigated the role of MMPs in neurological worsening of acute lacunar infarction. Forty-nine consecutive patients with an acute lacunar infarction (as defined by clinical and MRI criteria within 48 h after stroke onset) were evaluated. Clinical, biochemical, rheological, inflammatory and other parameters were compared between progressive and nonprogressive groups. Among the variables, only inflammatory parameters, including MMP-9 and erythrocyte sedimentation rate, were associated with neurological worsening of acute lacunar infarction (p < 0.05). These results suggest that the inflammatory process could play an important role in early neurological worsening of acute lacunar infarction.

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.

Received December 30, 2014 Revised March 16, 2015 Accepted March 16, 2015 Address for correspondence: A-Hyun Cho, MD, PhD Department of Neurology, Yeouido St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, 10 63-ro, Yeongdeungpo-gu, Seoul 150-713, Korea Tel: +82-2-3779-2433 Fax: +82-2-782-8654 E-mail: ahyun@catholic.ac.kr 급성열공뇌경색(acute lacunar infarct)과 미세뇌출혈(cerebral microbleeds)은 뇌소혈관질환이라는 유사한 병리기전을 공유한 다. 그러나 전자의 경우 혈관이 막히는 경우이고 후자의 경우 혈관벽을 통한 혈액의 누출이 발생한 경우이다. 따라서 두 개의 서로 다른 병리현상 및 영상소견이 함께 관찰되기는 어렵다. 최 근 영상기술의 발전으로 기울기에코영상(gradient echo image)을 통하여 미세뇌출혈을 관찰하고, 확산강조영상(diffusion-weighted image)을 통하여 급성열공경색을 쉽게 관찰할 수 있게 됨에 따 라 다양한 영상소견의 발견이 가능하다. 이에 저자들은 급성증

In acute lacunar infarction, MRI may overestimate eventual infarct size and the imaging evolution of acute lesions is not fully understood. Our objective was to examine eventual infarct size, the incidence of cavity formation, and factors associated with cavitation in patients presenting with acute lacunar infarction.Patients with acute diffusion-weighted imaging (DWI) infarcts ≤25 mm in diameter, in the distribution of a penetrating artery, who had a follow-up MRI or CT at least 1 month or longer from stroke onset were retrospectively included. We measured baseline lesion size on DWI and T2/fluid-attenuated inversion recovery (FLAIR) and follow-up lesion size on T2/FLAIR and CT. Follow-up MRI and CT images were assessed for cavity formation. Predictors for cavitation were assessed in a multivariate model.We identified 75 patients with lacunar infarction and follow-up CT or MRI, done 20.2 ± 16.6 and 21.2 ± 17.4 months after stroke, respectively. Mean baseline DWI size was 13.5 ± 5.7 and T2/FLAIR size was 13.1 ± 5.3 mm. Follow-up T2/FLAIR lesion size was 8.2 ± 3.4 mm and smaller than baseline DWI and T2/FLAIR (p =0.001). Follow-up whole lesion size on CT scan was 7.1 ± 4.1 and smaller than baseline DWI and T2/FLAIR (p = 0.001). Cavitation occurred in 23/38 (61%) MRI and 50/70 (70%) CT scans. We identified periventricular white matter lesions as a predictor of cavity formation by MRI and CT.Acute DWI significantly overestimates final infarct size. A third of lacunar infarcts do not develop a cavity.

Patients with acute lacunar infarction in the lenticulostriate artery (LSA) territory often show progression of motor deficits (PMD) after admission. The purpose of our study is to identify predictors for PMD using the findings of diffusion-weighted imaging (DWI) on admission.From January 2005 to December 2008, we studied 60 consecutive patients with acute lacunar infarction in the LSA territory within 24h after onset. To identify predictors for PMD, clinical characteristics including vascular risk factors and DWI findings were evaluated. DWI findings included the size and location of the infarcts and the slice numbers of infarcts visible on DWI. For the location, posterior type was defined as an infarct located in the posterior part of corona radiata on the second slice from the top among slices including corona radiata.Twenty-six patients (43%) showed PMD. In univariate analysis, ageor=75 (P=0.03), female sex (P=0.04), infarct slice numberor=3 (P=0.04), and posterior type infarct (P0.001) were more frequent in the PMD group than in the no PMD group. In multivariate analysis, posterior type infarct was the only independent predictor among DWI findings for PMD (odds ratio, 14.83; 95% confidence interval, 3.54-87.21, P0.001).Posterior type infarct was the independent predictor in DWI findings for PMD in patients with lacunar infarction in the LSA territory. We postulate that the posterior type infarct may affect the corticospinal tract to a greater degree and cause PMD.

Purpose: To correlate the findings of perfusion-weighted imaging (PWI) with clinical outcomes in patients with acute lacunar infarction. Materials and Methods: Eleven patients (7 males and 4 females) with acute lacunar infarction who were examined within 50 (mean, 29) hours of the onset of symptoms underwent conventional MRI, diffusion-weighted imaging (DWI) and PWI. Gadolinium (0.2 mmol/kg) was injected at a rate of 2 ml/sec, and PWI was performed using a gradient-echo EPI pulse sequence and the following parameters: TR/TE, 2000/60; flip angle, 90 degree; matrix size, 128128. Relative cerebral blood volume (rCBV) maps were derived from gadolinium bolus perfusion-weighted images where rCBV ratios between infarcted areas were detected by DWI, and contralateral control areas were obtained. In each case, the resulting rCBV ratio at a lesion site was compared with the clinical outcome determined on the basis of the difference between National Institute Health Stroke Scale (NIHSS) scores at admission and discharge. Results: With the aid of the time-intensity curve obtained at PWI, the rCBV maps revealed a hypoperfused area in 10 of 11 patients, and there was positive correlation (r=0.81) with clinical outcome. Conclusion: Although PWI has a lower detection rate than DWI, it may be a useful modality for helping determine prognosis in cases of acute lacunar infarction.

Thirty-one patients with presumed lacunar stroke, recent (18 patients) or remote (13 patients), were evaluated with brain magnetic resonance imaging (MRI). MRI detected small, deep lesions appropriate to symptoms in 23 of the patients (74%) and was diagnostically superior to brain computed tomography (CT) in those cases where both studies were obtained acutely. MRI also appeared useful in distinguishing between acute and chronic ischemic lesions. Especially in the setting of suspected acute lacunar infarction, MRI, when available, should replace CT as the diagnostic imaging procedure of choice.