Acute Lacunar Stroke Research Articles

Early neurological deterioration in acute lacunar ischemic stroke: Systematic review of incidence, mechanisms, and prospects for treatment.

Cerebral small vessel disease (CSVD) causes between 25% and 30% of all ischemic strokes. In acute lacunar ischemic stroke, despite often mild initial symptoms, early neurological deterioration (END) occurs in approximately 15-20% of patients and is associated with poor functional outcome, yet its mechanisms are not well understood. In this review, we systematically evaluated data on: (1) definitions and incidence of END, (2) mechanisms of small vessel occlusion, (3) predictors and mechanisms of END, and (4) prospects for the prevention or treatment of patients with END. We identified 67 reports (including 13,407 participants) describing the incidence of END in acute lacunar ischemic stroke. The specified timescale for END varied from <24 h to 3 weeks. The rate of END ranged between 2.3% and 47.5% with a pooled incidence of 23.54% (95% confidence interval (CI) = 21.02-26.05) but heterogeneity was high (I2 = 90.29%). The rates of END defined by National Institutes of Health Stroke Scale (NIHSS) decreases of ⩾1, ⩾2, ⩾3, and 4 points were as follows: 24.17 (21.19-27.16)%, 22.98 (20.48-25.30)%, 23.33 (16.23-30.42)%, and 10.79 (2.09-23.13)%, respectively, with lowest heterogeneity and greatest precision for a cutoff of ⩾2 points. Of the 20/67 studies (30%) reporting associations of END with clinical outcome, 19/20 (95%) reported worse outcomes (usually measured using the modified Rankin score at 90 days or at hospital discharge) in patients with END. In a meta-regression analysis, female sex, hypertension, diabetes, and smoking were associated with END. END occurs in more than 20% of patients with acute lacunar ischemic stroke and might provide a novel target for clinical trials. A definition of an NIHSS ⩾2 decrease is most used and provides the best between-study homogeneity. END is consistently associated with poor functional outcome. Further research is needed to better identify patients at risk of END, to understand the underlying mechanisms, and to carry out new trials to test potential interventions.

Analysis of events from sudden isolated dysarthria to diagnosis of myasthenic crisis: myasthenia gravis mimicking acute lacunar stroke—a case report

BackgroundMyasthenic crisis (MC) is a life-threatening complication of myasthenia gravis (MG), necessitating ventilation. Achieving a safe and timely diagnosis of myasthenic crisis with atypical, isolated presentation is a considerable challenge particularly in elderly patients, where myasthenia gravis can present with isolated dysarthria in rare instances, giving a clinical impression of lacunar stroke.Case presentationWe present a compelling case of a 73-year-old Caucasian female presenting with abrupt onset of isolated dysarthria. Despite initial treatment for a presumed lacunar stroke, subsequent evaluations led to her diagnosis of a myasthenic crisis. Within 72 h of admission, the patient developed dysphagia and shortness of breath, requiring supplemental oxygen. The case highlights the sequential progression of events from the atypical presentation of isolated dysarthria and its course to the management of a myasthenic crisis.ConclusionOur reported case focuses on the discussion of myasthenia that mimicked a lacunar stroke and was finally diagnosed at a critical time of medical crisis. This case highlights the imperative notion that isolated dysarthria in elderly individuals warrants vigilant monitoring for possible myasthenia gravis, given the low incidence of lacunar stroke presenting with only dysarthria.

Recurrent cerebrovascular events after recent small subcortical infarction

BackgroundRecent small subcortical infarcts (RSSI) are the neuroimaging hallmark feature of small vessel disease (SVD)-related acute lacunar stroke. Long-term data on recurrent cerebrovascular events including their aetiology after RSSI are scarce.Patients and methodsThis retrospective study included all consecutive ischaemic stroke patients with an MRI-confirmed RSSI (in the supply area of a small single brain artery) at University Hospital Graz between 2008 and 2013. We investigated associations between clinical and SVD features on MRI (STRIVE criteria) and recurrent cerebrovascular events, using multivariable Cox regression adjusted for age, sex, vascular risk factors and MRI parameters.ResultsWe analysed 332 consecutive patients (mean age 68 years, 36% women; median follow-up time 12 years). A recurrent ischaemic cerebrovascular event occurred in 70 patients (21.1%; 54 ischaemic strokes, 22 transient ischaemic attacks) and was mainly attributed to SVD (68%). 26 patients (7.8%) developed intracranial haemorrhage. In multivariable analysis, diabetes (HR 2.43, 95% CI 1.44–3.88), severe white matter hyperintensities (HR 1.97, 95% CI 1.14–3.41), and cerebral microbleeds (HR 1.89, 95% CI 1.32–3.14) on baseline MRI were related to recurrent ischaemic stroke/TIA, while presence of cerebral microbleeds increased the risk for intracranial haemorrhage (HR 3.25, 95% CI 1.39–7.59). A widely used SVD summary score indicated high risks of recurrent ischaemic (HR 1.22, 95% CI 1.01–1.49) and haemorrhagic cerebrovascular events (HR 1.57, 95% CI 1.11–2.22).ConclusionPatients with RSSI have a substantial risk for recurrent cerebrovascular events—particularly those with coexisting chronic SVD features. Recurrent events are mainly related to SVD again.

Abstract WP136: Impaired Venous Outflow Impacts Functional Outcomes in Acute Small Subcortical Infarcts: A Single-Center Retrospective Analysis

Introduction: Acute small subcortical infarcts (SSI), colloquially acute lacunar stroke, are a radiographic diagnosis representing a myriad of pathophysiologic processes. One such pathophysiologic subgroup is venous collagenosis which serves as a pathologic indicator that aberrant venous outflow may contribute to SSI development. We aimed to identify whether impaired venous outflow (IVO) impacted functional outcomes in individuals presenting with SSI. Methods: We performed a single-center retrospective study of individuals who presented to the Rhode Island Hospital Comprehensive Stroke Center. Included individuals were ≥ 18 years with the diagnosis of SSI, as defined per consensus criteria, on brain MRI diffusion weighted imaging. The primary exposure is the presence of impaired venous outflow (IVO) defined radiologically in accordance with prior studies, as hyperintensity of the jugular, sigmoid, or transverse sinuses along the skull base on MR angiogram time of flight, Figure. The primary outcome was a favorable function outcome at hospital discharge defined as a modified Rankin Scale (mRS) of ≤ 3. Standard descriptive and regression statistical techniques were used for data interpretation. Results: We identified 39 patients who met criteria with 12 (30.8%) with IVO. Age and vascular risk factors did not significantly differ amongst the cohort. Twenty-six (66.7%) had a favorable hospital discharge outcome favorable functional outcome with IVO being less common [IVO present: 5/26 (19.2%) versus LVO absent: 21/26, (80.8%), p = 0.034]]. After adjusting for age and hypertension, IVO was associated with an odds ratio of 8.33 (95%CI 1.41-49.3, p =0.019). Conclusion: We found that IVO may be an independent contributor to fewer favorable functional outcomes. This data highlights that not only the arterial vessels are of relevance in acute SSI.

Relationships of Hematocrit With Chronic Covert and Acute Symptomatic Lacunar Ischemic Lesions.

Red blood cell (RBC) concentrations are known to associate with ischemic stroke. It is unclear whether RBC concentrations associate specifically with small vessel disease lacunar infarcts. We investigated the hypothesis that RBC concentrations associate with both chronic covert and acute symptomatic brain MRI lacunar infarcts. A cross-sectional observational analysis was performed across 2 cohorts with available hematocrit (as the assessment of RBC concentration exposure) and MRI outcome data. The primary setting was a population-based cohort of stroke-free, older adult (>50 years) participants from the Northern Manhattan Study (NOMAS) enrolled between 2003 and 2009. A second replication sample consisted of patients admitted with acute stroke and enrolled into the Columbia Stroke Registry (CSR) between 2005 and 2020. Associations of hematocrit with (1) chronic, covert lacunar infarcts and (2) symptomatic (i.e., acute) lacunar strokes were separately assessed from the NOMAS and CSR cohorts, respectively, using general additive models after adjusting for relevant covariates. Of 1,218 NOMAS participants analyzed, 6% had chronic, covert lacunar infarcts. The association between hematocrit and these covert lacunar infarcts was U-shaped (χ2 = 9.21 for nonlinear associations; p = 0.03), with people with hematocrit extremes being more likely to have covert lacunar infarcts. Of the 1,489 CSR patients analyzed, 23% had acute lacunar strokes. In this sample, only the relationships of increased hematocrit concentrations and lacunar strokes were replicated (adjusted coefficient β = 0.020; SE = 0.009; p = 0.03). We identified relationships of hematocrit with MRI lacunar infarcts in both stroke-free and ischemic stroke cohorts, respectively. The relationship between increased hematocrit concentrations with lacunar infarcts was replicated in both cohorts. Further studies are required to clarify the mechanisms behind the relationships of hematocrit with ischemic cerebral small vessel disease.

Ischemic stroke following COVID-19 vaccination

Following the coronavirus disease 2019 (COVID-19) vaccination, complications are expected. In this regard, coagulopathy after COVID-19 vaccination has been reported. Here, we report a rare case of ischemic stroke subsequent to receiving the Beijing Bio-Institute of Biological Products - Coronavirus (BBIBP-CorV) vaccine (Sinopharm). Ten days after receiving the first dose of the BBIBP-CorV vaccine, a 76-year-old woman showed right central hemifacial weakness, balance disorder, and right hemisensory involvement with normal muscle force. Although the magnetic resonance imaging assessment revealed an acute lacunar stroke in her left thalamus, laboratory findings were normal. Based on our report, ischemic stroke may be a post-complication of BBIBP- CorV vaccination. However, further studies are needed to confirm this finding.

Regional white matter hyperintensity volume predicts persistent cognitive impairment in acute lacunar infarct patients.

White matter hyperintensity (WMH) is often described in acute lacunar stroke (ALS) patients. However, the specific relationship between regional WMH volume and persistent cognitive impairment remains unclear. We enrolled patients with ALS who were hospitalized at the First Affiliated Hospital of Soochow University between January 2020 and November 2022. All patients were assessed for global cognitive function using the Montreal Cognitive Assessment (MoCA) scale at 14 ± 2 days and 6 months after the onset of ALS. Manifestations of chronic cerebral small vessel disease (CSVD) were assessed via MRI scan. The distributions of regional WMH were segmented, and their relationship with cognitive impairment was evaluated. A total of 129 patients were enrolled. Baseline frontal WMH volume (OR = 1.18, P = 0.04) was an independent risk factor for long-term cognitive impairment after ALS. Furthermore, the presence of WMH at the genu of the corpus callosum (GCC) at baseline (OR = 3.1, P = 0.033) was strongly associated with persistent cognitive decline. Multivariable logistic regression analysis showed that depression (OR = 6.252, P = 0.029), NIHSS score (OR = 1.24, P = 0.011), and albumin at admission (OR = 0.841, P = 0.032) were also important determinants of long-term cognitive impairment after ALS. Our study found that WMH, especially frontal WMH volume and the presence of WMH at the GCC at baseline, independently contributed to long-term cognitive decline in ALS patients. This study provides new evidence of the clinical relationship between regional WMH volume and cognitive impairment in ALS patients.

Prevalence and predictive factors of progression in pure motor, ataxic hemiparesis and mixed sensorimotor lacunar syndrome

Objectives: To explore the prevalence and predictive factors of progressive lacunar stroke (PLS). Methods: Consecutive patients with acute lacunar stroke, who were admitted at King Chulalongkorn Memorial hospital during 1st July 2015-30th June 2018, were retrospectively recruited. The clinical lacunar stroke was defined as acute motor deficit lasting more than 24 hours and clinical syndrome compatible with pure motor hemiparesis, ataxic hemiparesis or sensorimotor stroke. The patients with cardioembolism or imaging shown cortical involvement was excluded. PLS was considered if there was an increase in NIHSS more than 2 points during admission. Patient characteristics, clinical data, imaging findings and medical treatment during admission was statistically analyzed. Functional outcome was assessed based on the modified Rankin Scale at discharge and 3 months. Results: Of 302 patients, 70 (23.2%) had PLS. Multivariate logistic regression analysis revealed that age at stroke onset more than 60 years (adjusted odd ratio [aOR], 2.17; 95% confidence interval [CI], 1.16-4.06, p=0.016), initial systolic blood pressure (SBP) more than 165 mmHg (aOR 2.40, 95%CI 1.25-4.61, p=0.008), white blood cell (WBC) more than 8500/ microliters (aOR 1.95, 95%CI 1.05-3.62, p=0.034), pontine infarction (aOR 1.99, 95%CI 1.07-3.71, p=0.031), branch atheromatous disease (BAD) (aOR 2.47, 95%CI 1.37-4.48, p=0.003), and significant vessels stenosis relevant to infarction (aOR 2.41, 95%CI 1.09-5.36, p=0.031) were independent predictors of PLS. Conclusion: Age more than 60 years, initial SBP more than 165mmHg, WBC more than 8500/microliters, pontine infarction, BAD and significant symptomatic artery stenosis are associated with PLS.

Abstract WP188: Relationships Of Hematocrit With Asymptomatic And Symptomatic Lacunar Ischemic Lesions

Introduction: Hematocrit at both low and high extremes can result in both hypoxia and thrombosis respectively. While both scenarios may predispose to ischemia, it is unclear whether hematocrit associates with small vessel cerebrovascular lacunar infarcts. Hypothesis: Hematocrit levels will associate with both asymptomatic and symptomatic cerebrovascular lacunar infarcts in stroke-free participants and ischemic stroke patients, respectively. Methods: A cross sectional observational analysis of a prospective, population-based cohort study of stroke-free, older adult (&gt;50) participants from the Northern Manhattan study (NOMAS) receiving baseline hematocrit testing and MRI between 2003-2008 were analyzed. A second, single center prospective cohort of admitted adult ischemic stroke patients receiving baseline hematocrit testing and MRI between 2005-2018 was evaluated. Associations of hematocrit with covert, asymptomatic chronic lacunar infarcts from stroke-free participants in NOMAS were assessed using general additive models after adjusting for relevant covariates. Separate analyses were performed to assess associations of hematocrit with symptomatic acute lacunar infarct stroke etiology using similar adjusted models for patients admitted and enrolled into the ischemic stroke registry. Results: Of 1218 NOMAS participants analyzed, 6% had covert chronic lacunar infarcts. The association between hematocrit and covert chronic lacunar infarcts was U-shaped (X2: 9.21; p-value: 0.03). In the 1489 patients from the ischemic stroke registry, 23% were identified to have symptomatic acute lacunar infarcts. Linear relationships were identified with higher hematocrit and symptomatic acute lacunar infarct etiology (adjusted coefficient beta: 0.020; standard error: 0.009; p=0.03). Conclusions: We identified relationships of hematocrit with both asymptomatic and symptomatic lacunar infarcts in both stroke-free and ischemic stroke cohorts, respectively. There may be a relevant role of red blood cell volumes with ischemic cerebral small vessel disease pathophysiology. However, further studies are required to clarify the mechanisms behind these relationships.

The Correlation of Glial Fibrillary Acid Protein Level to Cognitive Function Outcome in Acute Lacunar Ischemic Stroke Patient

ABSTRACT :&#x0D; Introduction : Glial fibrillary acidic protein (GFAP) is a filamentous protein found in central nervous system astrocytes. Increased serum GFAP levels are caused by the process of astrogliosis after ischemic stroke and are associated with multisynaptic disorders so that they are at risk of causing cognitive disorders.&#x0D; Objective: To analyze the correlation between GFAP levels and cognitive function output in acute lacunar ischemic stroke patients.&#x0D; Research Methods : Analytical observational with prospective cohort approach. The subjects of this study were Acute lacunar ischemic stroke patients with mild to moderate NIHSS scores. Serum GFAP levels were taken at the onset of 48-72 hours of stroke. Cognitive function was measured using the Indonesian version of MoCA (MoCA Ina) test on the seventh and thirtieth day. Bivariate and multivariate analyzes were performed to assess the correlation between GFAP levels, cognitive functions and the confounding factors.&#x0D; Results: There was a significant correlation between GFAP levels and the MoCA Ina scores on the seventh day (r= -0.32, p=0.044), the thirtieth day (r= -0.398, p=0.011), and improvement in MoCA Ina scores (r= -0.342, p = 0.031). There was a significant correlation between GFAP levels on the executive domain on the seventh day (p= 0.01) and thirtieth day (p= 0.005), visuospatial on seventh day (p= 0.004) and thirtieth day (p= 0.016), language on the thirtieth day (p = 0.005), and memory on thirtieth day (p= 0.001). There was no significant correlation between GFAP levels and improvements in attentional, memory, language, visuospatial, and executive domains.&#x0D; Conclusion: There was a significant correlation between GFAP levels and MoCA Ina scores on the seventh, thirtieth day and the improvement of MoCA Ina scores. There was a significant correlation between GFAP levels with the executive, visuospatial, language, and memory domains.&#x0D; Keywords: cognitive, GFAP, lacunar ischemic stroke, MoCA Ina

Is the female sex associated with an increased risk for long-term cognitive decline after the first-ever lacunar stroke? Prospective study on small vessel disease cohort.

Sex is a significant determinant of survival and functional outcome after stroke. Long-term cognitive outcome after acute lacunar stroke in the context of sex differences has been rarely reported. A cohort of small vessel disease (SVD) patients presenting with first-ever acute lacunar stroke and normal cognitive status has been evaluated 4 years after the qualifying event for the presence of cognitive impairment (CI) with a comprehensive neuropsychological battery. Differences in baseline clinical and neuroimaging characteristics were compared between sexes in relation to cognitive status. A total of 124 female and 150 male patients were analyzed. No difference was detected between the groups regarding age (p = 0.932) or frequency of common vascular risk factors (p > 0.1 for all). At the baseline assessment, women had more disabilities compared to men with a mean modified Rankin scale (mRS) score of 2.5 (1.5 in men, p < 0.0001). Scores of white matter hyperintensities (WMH) of presumed vascular origin and a total number of lacunes of presumed vascular origin on brain MRI were higher in women compared to men (p < 0.0001 for all). As many as 64.6% of patients had CI of any severity on follow-up, women more frequently (77.4%) than men (54.0%; p < 0.0001). Univariate logistic regression analysis showed that female sex, higher NIHSS and mRS scores, presence of depression, and increasing WMH severity were associated with an increased risk for CI. Multivariate regression analysis indicated that only depression (OR 1.74, 95%CI 1.25-2.44; p = 0.001) and WMH severity (OR 1.10, 95%CI 1.03-1.17; p = 0.004) were independently associated with the CI. At the long-term follow-up, women lacunar stroke survivors, compared to men, more frequently had CI in the presence of more severe vascular brain lesions, but this association was dependent on the occurrence of depression and severity of WMH, and could not be explained by differences in common vascular risk factors.

本邦の1次脳卒中センターにおける穿通枝梗塞の急性期治療に関するアンケート調査

【背景と目的】穿通枝梗塞，特にbranch atheromatous disease（BAD）は，治療にもかかわらずしばしば神経症状が増悪するが，有効な治療戦略は確立されていない．本邦の穿通枝梗塞の急性期治療方針を明らかにする．【方法】1次脳卒中センター500施設に臨床情報，穿通枝梗塞の画像を複数例提示し，各症例における治療方針を尋ねた．【結果】38%の施設から回答を得た．発症6時間，NIHSS 3点のBAD型梗塞では，初期治療として約70%は抗凝固薬+抗血小板薬2剤以上の多剤併用療法を選択し，症状増悪時に約50%で抗血栓薬を追加すると回答した．発症2時間のBAD型梗塞では，87%でrt-PA静注療法を行い，その後の早期症状増悪時には35%が24時間以内に抗血栓薬を再開すると回答した．【結論】本邦ではBAD型梗塞に対して，現行のガイドラインの推奨より強力な抗血栓療法が行われている可能性がある．

Risk factors related to early neurological deterioration in lacunar stroke and its influence on functional outcome.

To identify risk factors for early neurological deterioration (END) in acute lacunar stroke patients and its influence on functional outcome. Consecutive acute lacunar stroke patients defined by magnetic resonance imaging (MRI) between January 2018 and June 2020 were included in the study. END was defined as any persisting increase in National Institutes of Health Stroke Scale (NIHSS) score of ⩾ 2 points post admission, and favorable outcome was defined as a modified Rankin Scale (mRS) of 0-2 at discharge. Univariable and multivariable logistic regression were performed to identify risk factors related to END, as well as the influence of END on functional outcome. Among a total of 638 lacunar stroke patients (420 males (65.8%), median age 66 years (interquartile range (IQR): 56-74)), 108 (16.9%) developed END, and 94.4% (102/108) of the END occurred within 72 h post admission. Admission NIHSS score (adjusted odds ratio (aOR) 1.132, 95% confidence interval (CI) 1.046-1.225, p = 0.002), female (aOR 2.752, 95% CI 1.277-5.933, p = 0.010), admission systolic blood pressure (SBP) (160-179 mm Hg) (aOR 9.395, 95% CI 4.310-20.479, p < 0.001) and admission SBP (⩾180 mm Hg) (aOR 16.030, 95% CI 5.991-42.891, p < 0.001) were significantly associated with END. Delay time from onset to admission (aOR 0.995, 95% CI 0.990-1.000, p = 0.031), SBP dropping (⩾20 mm Hg) within 3 days or when END occurred (aOR 0.037, 95% CI 0.016-0.086, p < 0.001) and thalamic lacunar infarction (aOR 0.098, 95% CI 0.012-0.827, p = 0.033) were inversely associated with END. END (aOR 12.374, 95% CI 6.881-22.254, p < 0.001) and higher admission NIHSS score (aOR 1.488, 95% CI 1.359-1.629, p < 0.001) predicted unfavorable outcome at discharge. END in lacunar stroke patients is common and is associated with unfavorable outcome. Admission high SBP is a potentially modifiable risk factor for prevention of END, but this needs further investigation.

Heterogeneity of White Matter Hyperintensity and Cognitive Impairment in Patients with Acute Lacunar Stroke.

The severity of white matter hyperintensity (WMH) in patients with acute lacunar stroke (ALS) may be not completely parallel to cognitive impairment. Controversies persist about the effects of WMH on cognitive dysfunction. It is vital to explore whether the association may be affected by certain factors and whether a subsequent subgroup analysis is necessary. The aim of this study was to evaluate the relationship between WMH and cognitive impairment in acute lacunar stroke patients and the possible causal factors. We continuously enrolled patients with ALS who were hospitalized at the First Affiliated Hospital of Soochow University between October 2017 and June 2022. The cognitive function of all patients was assessed by using the Montreal Cognitive Assessment (MoCA) scale 14 ± 2 days after the onset of AIS, and the results were adjusted to the education level. The MoCA scale was reevaluated at the 6-month (day 182 ± 7) follow-up by outpatient visit or video. Demographic and clinical data were collected. The manifestations of chronic cerebral small-vessel disease (CSVD), including the total Fazekas score and total CSVD burden score, were assessed with an MRI scan. A mismatch refers to an inconsistency between the severity of WMH and cognitive dysfunction. A Type 1 mismatch refers to cognitive impairment with mild WMH (total Fazekas score = 0-1), and a Type 2 mismatch refers to severe WMH (total Fazekas score = 5-6) in patients with normal cognitive function. Among 213 enrolled ALS patients, 66 patients (31.0%) had cognitive dysfunction, and 40 patients (18.8%) had mismatches. Twenty-seven cases (12.7%) were Type 1 mismatched, and seventeen cases (8.0%) were Type 2 mismatched. Age, gender, fibrinogen and cerebral infarction history were independent risk factors for cognitive impairment in ALS patients. Imaging features, including moderate to severe WMH, deep WMH and the total CSVD burden score, were also independently associated with cognitive impairment. The patients in the mismatched group were older, had more severe deep WMH and had a higher occurrence of depression (p &lt; 0.05). The NIHSS score, depression and microbleeds were significantly different between the Type 1 mismatched group and the matched group (p = 0.018, p = 0.012 and p = 0.047). Patients in the Type 2 mismatched group were male (p = 0.04), had a lower level of fibrinogen (p = 0.005), a lower incidence of CMBs (p = 0.003), a lower total CSVD burden score (p = 0.017), more severe paraventricular WMH (p = 0.035) and milder deep WMH (p = 0.026). Our study examined a homogeneous study cohort of recruited patients with symptomatic ALS. We found heterogeneity between WMH and cognitive function in ALS patients. Despite a similar WMH severity, some baseline clinical features and other conventional CSVD imaging characteristics may account for this heterogeneity phenomenon. Our findings provide data for the early diagnosis and prevention of cognitive impairment in ALS patients and suggest that the severity of WMH is not completely parallel to cognitive impairment. The white matter microstructural injury and remote WMH effects may account for the mismatch phenomenon. More attention should be paid to understanding the underlying mechanisms and finding new imaging markers.

Editors' Note: Early Neurologic Deterioration in Lacunar Stroke: Clinical and Imaging Predictors and Association With Long-term Outcome

Early neurologic deterioration (END) is a frequent complication of acute ischemic stroke and is often due to progressive tissue infarction. In their single-center analysis of acute lacunar stroke identified on magnetic resonance imaging (n = 365), Dr. Vynckier and colleagues report 16.7% of patients experienced a worsening of 2 or more points in the NIH Stroke Scale within 24 hours of arrival and were classified as having END. It is important that milder stroke severity, ventral pontine injury, capsular warning syndrome, and hypoperfusion on baseline imaging were predictive of END. Dr. Alpert comments that early mobilization—while important for expediting rehabilitation and discharge—may increase the risk of END. Dr. Zini and colleagues also highlight the putative relationship between END and branch atheromatous disease, which may be targeted with combination antiplatelet therapy. Indeed, the study by Vynckier et al. found that acute dual antiplatelet therapy was associated with a 90% lower chance of END (adjusted odds ratio 0.10, 95% CI 0.01–0.89). Dual antiplatelet therapy may be useful for preventing progressive tissue infarction in lacunar disease; however, this can only be confirmed in a randomized clinical trial. Early neurologic deterioration (END) is a frequent complication of acute ischemic stroke and is often due to progressive tissue infarction. In their single-center analysis of acute lacunar stroke identified on magnetic resonance imaging (n = 365), Dr. Vynckier and colleagues report 16.7% of patients experienced a worsening of 2 or more points in the NIH Stroke Scale within 24 hours of arrival and were classified as having END. It is important that milder stroke severity, ventral pontine injury, capsular warning syndrome, and hypoperfusion on baseline imaging were predictive of END. Dr. Alpert comments that early mobilization—while important for expediting rehabilitation and discharge—may increase the risk of END. Dr. Zini and colleagues also highlight the putative relationship between END and branch atheromatous disease, which may be targeted with combination antiplatelet therapy. Indeed, the study by Vynckier et al. found that acute dual antiplatelet therapy was associated with a 90% lower chance of END (adjusted odds ratio 0.10, 95% CI 0.01–0.89). Dual antiplatelet therapy may be useful for preventing progressive tissue infarction in lacunar disease; however, this can only be confirmed in a randomized clinical trial.

Hemichorea as initial presentation of newly diagnosed diabetes and acute lacunar stroke

Hemichorea is one of the spectrums of involuntary, continuous, non-purposeful movement of one side of the body, a choreiform disorder. Hemichorea causes vary and include various inherited or acquired systemic conditions. There might be overlapping pathophysiology where the synergistic effects of uncontrolled hyperglycemia and vascular insufficiency cause an incomplete transient dysfunction of the striatum, leading to hemichorea. We herein describe a patient who presented with hemichorea triggered by hyperglycemia and was incidentally found to have an acute lacunar stroke. She was initiated on insulin with good glycemic control. Secondary stroke prevention therapy with aspirin and statin was also started. Her symptoms improved inpatient after stable glycemic control was achieved. After 3 months, her symptoms had completely resolved. Hemichorea is an unusual initial presentation for newly diagnosed diabetes mellitus or stroke. Hence, recognizing and diagnosing this uncommon disease entity is pertinent to make a timely and accurate diagnosis, which can lead to a rapid clinical response.

Thyroid Function Affects the Risk of Post-stroke Depression in Patients With Acute Lacunar Stroke.

ObjectiveThis study aimed to investigate whether thyroid function profiles are associated with post-stroke depression (PSD) and evaluate the mediation effect of cerebral small vessel disease (cSVD) on the association of thyroid function profiles and PSD in patients with acute ischemic lacunar stroke.MethodsIn this study, 372 patients with confirmed acute ischemic lacunar stroke within 3 days of onset were consecutively recruited. Serum levels of thyroid hormones and thyroid antibodies were detected on admission. Lacunar infarcts, white matter lesions, cerebral microbleeds, and enlarged perivascular spaces were rated using validated scales. The severity of depression was scored with the 24-item Hamilton Depression Scale in the hospital after a week of stroke onset. Multivariate regression was utilized to analyze the association of thyroid function profiles and PSD. Mediation analysis was employed to evaluate the effect of cSVD on the association of thyroid function profiles and PSD.ResultsA total of 87 (23.4%) participants were diagnosed with depression after stroke. Serum thyroid-stimulating hormone (TSH) levels were significantly higher in patients with PSD than in those without PSD, while free triiodothyronine (FT3) and free thyroxine (FT4) were not significantly different between the two groups. After adjusting for potential confounders, serum TSH levels were positively associated with the risk of PSD (OR = 1.228; 95% CI: 1.053–1.431, p = 0.009). A similar association was also found between the total cSVD burden score and PSD (OR = 2.137; 95% CI: 1.634–2.793, p < 0.001). Further mediation analysis indicated that 26.37% of the association between TSH and PSD was mediated by cSVD.ConclusionsSerum TSH levels on admission can probably predict depression after acute ischemic lacunar stroke.

Abstract TP96: Mild Luminal Stenosis Of Parent Artery And Neurologic Deterioration After Acute Lacunar Stroke

Introduction: Neurologic deterioration (ND) occurs in a quarter of acute lacunar infarcts and may lead to severe disability, but underlying pathophysiology of ND remains poorly understood. We sought to identify risk factors and clinical characteristics associated with ND. Methods: This retrospective observational study included consecutive patients with acute lacunar stroke admitted to New York University Langone Health and Brown University (NYU/Brown). Lacunar stroke was defined as a subcortical infarct &lt;1.5 cm on CT or &lt;2 cm on diffusion-weighted imaging without significant stenosis (&gt;50%) in the parent vessel and no cardioembolic source. We defined ND as any neurologic deterioration referable to the lacunar stroke and not related to a medical or non-cerebrovascular neurological complication. We used logistic regression analyses to determine associations between ND and luminal stenosis (&lt;50%) vs no luminal stenosis, after adjustment for key confounders. Furthermore, we attempted to validate findings using the Columbia University (CU) stroke registry and perform a meta-analysis combining the derivation and validation groups due to expected small samples and event rates. Results: The NYU/Brown sample included 205 patients, of whom 41 (20%) had ND. In adjusted models, we found no definite association between luminal stenosis and ND (aOR 1.74, 95% CI 0.73-4.14). From CU, 361 total patients were included, of whom 59 (16%) had ND. In adjusted models, we found an association between luminal stenosis and ND (aOR 2.28 95% CI 1.15-4.50). Meta-analysis of both cohorts found luminal stenosis associated with ND (RR [95% CI]: 1.75 [1.23-2.49]). Conclusions: In this multi-center study, luminal stenosis (&lt;50%) may be associated with ND following an acute lacunar infarct. Larger studies using high-resolution vascular imaging modalities such as vessel wall imaging are needed to validate our findings.

Case Report : Mr. I 56 years old with Stroke Non Hemoragic

Stroke is one of the most common diseases that cause functional impairment and disability. Stroke is the second leading cause of death and the leading cause of disability worldwide. Its incidence is increasing as the population ages. In addition, more young people have strokes in low- and middle-income countries. Data in Indonesia shows that stroke is the third most common cause of death, followed by diabetes mellitus and hypertension with a mortality rate of 138,268 people or 9.7% of the total deaths. Indonesia has a double burden in dealing with health problems. Lacunar strokes, a type of ischemic stroke, are small and located in non-cortical areas. Lacunar infarctions are caused by occlusion of small branches penetrating within the cerebral vessels of the circle of Willis, including branches of the middle cerebral artery, anterior cerebral artery, posterior cerebral artery, or spinal cord. basilar artery. The principle of treatment for acute lacunar stroke is very similar to that of acute ischemic stroke. The initial goals of acute stage treatment are to ensure medical stability and determine candidacy for thrombolysis. Tissue plasminogen activator (TPA) improves outcomes for patients with ischemic stroke. Once intracerebral hemorrhage has been ruled out, intravenous thrombolysis is an important step in treatment. Acute lacunar infarction is efficiently treated with TPA. This case report discusses a 56 year old Mr I diagnosed with a non-hemorrhagic stroke.

Mild Luminal Stenosis of Parent Artery and Neurologic Deterioration After Acute Lacunar Stroke

Background Early neurologic deterioration (END) occurs in a quarter of acute lacunar infarcts, but the underlying pathophysiological features are poorly understood. We sought to determine the association between luminal stenosis (&lt;50%) of the parent artery and END. Methods This observational study included consecutive patients with lacunar stroke from the ischemic stroke registries of New York University Langone Health and Brown University. All included patients were admitted for acute lacunar stroke, which was defined as a subcortical infarct &lt;1.5 cm on computed tomography or &lt;2 cm on diffusion‐weighted imaging without significant stenosis (&gt;50%) in the parent vessel and no cardioembolic source. We defined END as any neurologic deterioration referable to the acute lacunar stroke and not related to a medical or noncerebrovascular neurological complication. We used univariate and logistic regression analyses to determine associations between luminal stenosis (&lt;50%) and the odds of END. Furthermore, we attempted to validate findings using the Columbia University Medical Center stroke registry and perform a meta‐analysis combining the derivation and validation groups because of the expected small samples and event rates. Results The New York University Langone Health and Brown University sample included 205 patients, of whom 41 (20%) had END. In adjusted models, we found no definite association between luminal stenosis (&lt;50%) and END (adjusted odds ratio [OR], 1.74; 95% CI, 0.73–4.14). From Columbia University Medical Center, 361 total patients were included, of whom 59 (16%) had END. In adjusted models, we found an association between luminal stenosis (&lt;50%) and END (adjusted OR, 2.28; 95% CI, 1.15–4.50). Meta‐analysis of both cohorts found luminal stenosis (&lt;50%) associated with END (relative risk, 1.69; 95% CI, 1.17–2.43). Conclusions In this multicenter study, luminal stenosis (&lt;50%) may be associated with END following an acute lacunar infarct. Larger studies using vessel wall imaging are needed to validate our findings.