Little Association between Intracranial Arterial Stenosis and Lacunar Stroke (original) (raw)
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Cerebrovascular Diseases, 2007
Background: Lacunar stroke has been defined as an infarct <15 mm in diameter in the presence of symptoms of lacunar syndromes. We investigated a new approach in predicting whether a deep infarct is caused by small arterial occlusion. Methods: A total of 319 consecutive patients with acute symptomatic infarcts within the striatocapsular territory underwent diffusion-weighted imaging (DWI) and diagnostic workups, including vascular and cardiological studies. Predictors for nonlacunar mechanisms were evaluated by logistic regression analysis, with the size of infarct (1-mm increase) and stroke syndrome (traditional vs. atypical lacunar syndrome vs. cortical syndrome) graded rather than dichotomized. Results: Amongst the 171 patients who did not meet the established criteria for lacunar stroke, that is, deep infarct of ≧15 mm or presenting symptoms of nontraditional lacunar syndrome, a documented etiology could not be determined in 97 (56.7%) patients. In contrast, amongst the 148 pa...
Prevalence and Clinical Characteristics of Lacunar Stroke: A Hospital-Based Study
2021
Lacunar stroke (LS) is responsible for one-quarter of the overall number of ischemic strokes with long-term complications and carries health and economic issues for patients and health care systems. Therefore, we aimed to investigate lacunar versus non-lacunar strokes in a tertiary academic center. From February 2016 to July 2019, all patients admitted to the stroke unit were retrospectively reviewed. We included LS patients and compared them to other TOAST subtypes. Hemorrhagic stroke and conditions mimicking stroke were excluded. Regression analysis was done to determine LS predictors and outcomes. A 35.5% rate of LS among 989 ischemic stroke patients was found. Most patients (71.9%) were males. Lower National Institutes of Health Stroke Scale (NIHSS) scores at admission and negative history for cardiac diseases were predictors for LS in our population. At discharge, LS patients had low NIHSS scores and shorter hospitalization periods compared to non-LS patients. In conclusion, LS was prevalent among ischemic stroke patients in our cohort. Future studies are highly needed with long follow-up intervals to identify the stroke recurrence, complications, and outcomes.
Clinical Diagnosis of Lacunar Stroke in the First 6 Hours After Symptom Onset
Stroke, 2007
Background and Purpose— Although the pathophysiological heterogeneity of stroke may be highly relevant to the development of acute-phase therapies, discriminating between ischemic stroke subtypes soon after onset remains a challenge. We conducted a study of the accuracy of a clinical diagnosis of lacunar stroke in the first 6 hours after symptom onset. Methods— We analyzed data from 1367 patients in the Glycine Antagonist In Neuroprotection (GAIN) Americas trial. The Trial of ORG10172 in Acute Stroke Treatment (TOAST) category “small vessel (lacunar)” disease at day 7 or at hospital discharge was used as the reference standard to determine the accuracy of a diagnosis of a lacunar stroke made within 6 hours of symptom onset using the Oxfordshire Community Stroke Project (OCSP) classification “LACS.” Outcome was analyzed by comparing the proportions of patients classified as “LACS” at baseline or “small vessel (lacunar)” at 7 days who were dead or dependent at 3 months. Results— The p...
Should computed tomography appearance of lacunar stroke influence patient management?
Journal of Neurology, Neurosurgery & Psychiatry, 1999
Patients with a lacunar stroke syndrome may have cortical infarcts on brain imaging rather than lacunar infarcts, and patients with the clinical features of a small cortical stroke (partial anterior circulation syndrome, PACS) may have lacunar infarcts on imaging. The aim was to compare risk factors and outcome in lacunar syndrome (LACS) with cortical infarct, LACS with lacunar infarct, PACS with cortical infarct, and PACS with lacunar infarct to determine whether the clinical syndrome should be modified according to brain imaging.
Advances in Understanding the Pathophysiology of Lacunar Stroke: A Review
JAMA Neurology, 2018
S troke is the second leading cause of death in the world and the leading cause of disability in the United States. 1 Among ischemic strokes, there are different subtypes, including large artery atherosclerosis, cardioembolism, and cerebral small vessel disease (CSVD). Although CSVD has several clinical and radiographic manifestations, lacunar stroke (LS) is prototypical and accounts for 20% to 30% of ischemic strokes. 2,3 Clinically, LS can manifest with several syndromes depending on lesion location. 4 Silent LSs are found in 20% to 50% of healthy elderly people. 5 Lacunar strokes are particularly burdensome, with a 20% recurrence rate, 25% five-year mortality, and associated morbidities, such as vascular cogni-tive impairment. 3 Lacunar strokes, appropriately named given their propensity to form cavities (lacunes), were first described in 1838 (Figure 1). 3 More recently, the Standards for Reporting Vascular Changes on Neuroimaging definitions were developed to standardize terms that describe the appearance of sequelae of CSVD, including recent small subcortical infarcts, lacunes, white matter hyperin-tensities (WMHs), perivascular spaces, microbleeds, and brain atrophy, on imaging. 6 Lacunar strokes primarily encompass 2 terms: recent small subcortical infarcts, defined as recent infarc-tions in the territory of 1 perforating arteriole with imaging features or clinical symptoms consistent with occurrence in the previous few weeks, and lacunes, defined as round or ovoid, sub-cortical, fluid-filled cavities 3 to 15 mm in diameter, consistent with previous acute small subcortical infarcts or hemorrhages in the territory of 1 perforating arteriole. 6 Although this review focuses on LS, other abnormalities that result from CSVD are relevant because there are interrelated mechanisms and treatment implications. For example, recent small subcortical infarcts can also contribute to WMH, 3 and many intracerebral hemorrhages (ICHs) likely result from similar vessel abnormalities. 7 This suggests that patients with LS may have an increased risk for bleeding when taking antithrombotic medications. IMPORTANCE Stroke is the second leading cause of death in the world, and nearly one-third of ischemic strokes are lacunar strokes (LSs) or small subcortical infarcts. Although smaller in size, they create large problems, leaving many patients with intellectual and physical disabilities. Because there are limitations in understanding the underlying pathophysiology of LS, the development of novel therapies has been slow. OBSERVATIONS When the term lacune was described in the 1800s, its underlying pathophysiological basis was obscure. In the 1960s, C. Miller Fisher, MD, performed autopsy studies that showed that vessels supplying lacunes displayed segmental arteriolar disorganization, characterized by vessel enlargement, hemorrhage, and fibrinoid deposition. For these pathologic changes, he coined the term lipohyalinosis. Since that time, few attempts have been made to reconcile this pathologic description with modern mechanisms of cerebral small vessel disease (CSVD). During the past 6 years, progress has been made in understanding the clinical mechanisms, imaging characteristics, and genetic basis of LS. CONCLUSIONS AND RELEVANCE Questions persist regarding the order of events related to the initiation and progression of CSVD, how LS is related to other sequelae of CSVD, and whether LS is part of a systemic disease process. The relative roles of aging, oxidative stress, mechanical stress, genetic predisposition, and other vascular risk factors should be further studied, especially in the era of widespread antihypertensive use. Although understanding of endothelial dysfunction has increased, future work on the role of media and adventitial dysfunction should be explored. Recent advances in mapping the brain vasculome may generate new hypotheses. The investigation of new therapeutic targets, aimed at reversing CSVD processes and promoting neural repair after LS, depends upon further understanding these basic mechanisms.
Comparative Study of Risk Factors Between Lacunar and Non-lacunar Ischemic Strokes
Bangladesh Journal of Neuroscience, 2013
Background: Stroke is a leading cause of mortality and morbidity in both developed as well as developing countries The risk factors in lacunar stroke differ in comparison to nonlacunar strokes. In this study risk factors of lacunar stroke in comparison to non-lacunar were evaluated. Objectives: The aim of the study was to compare the risk factors among lacunar stroke and non-lacunar stroke. Methodology: This comparative study conducted in the department of Medicine and Neurology, Dhaka Medical College Hospital, Dhaka from September 2010 to August 2011. MRI of brain was done in 151 patients above 18 years of age with ischemic stroke and Lacunar stroke was found in 31 patients and non-lacunar stroke was detected in 120 patients. Based on the inclusion and exclusion criteria from them 30 patients with lacunar stroke were selected as Group-A patients and equal number of non-lacunar stroke same ages as group B were compared of. The risk factors of stroke were defined as hypertension, dia...
High risk of early neurological worsening of lacunar infarction
Acta Neurologica Scandinavica, 2018
Background and Purpose We aimed to evaluate factors associated with neurological worsening among patients with lacunar or non-lacunar infarction admitted within 3 hours and between 3-24 hours after stroke onset. Methods All patients admitted to Haukeland university hospital between 2006-2016 with acute cerebral infarction on MRI and admission within 24 hours were included. Repeated National Institute of Health Stroke Scale (NIHSS) scoring was performed in all patients whenever possible. Neurological worsening during the hospital stay was defined as NIHSS score increase ≥3 compared to NIHSS score on admission. Results In patients with lacunar infarction admitted within 3 hours of onset neurological worsening was associated with low NIHSS score on admission, low body temperature and leukoaraiosis whereras only internal carotid artery stenosis or occlusion was associated with neurological worsening in non-lacunar infaction. For patients admitted 3-24 hours after onset neurological worsening was associated with low body temperature, high systolic blood pressure and short time from onset to admission in patients with lacunar infarction, whereas high systolic blood pressure, high NIHSS score on admission, middle cerebral artery occlusion and high blood glucose were associated with neurological worsening in patients with non-lacunar infarction (all P<.05). Conclusions Lacunar infarctions with minor neurological deficits within 3 hours of stroke onset are at high risk of neurological worsening especially if concomitant low body temperature and leukoaraiosis.
International Journal of Molecular Sciences, 2022
Lacunar infarcts represent one of the most frequent subtypes of ischemic strokes and may represent the first recognizable manifestation of a progressive disease of the small perforating arteries, capillaries, and venules of the brain, defined as cerebral small vessel disease. The pathophysiological mechanisms leading to a perforating artery occlusion are multiple and still not completely defined, due to spatial resolution issues in neuroimaging, sparsity of pathological studies, and lack of valid experimental models. Recent advances in the endovascular treatment of large vessel occlusion may have diverted attention from the management of patients with small vessel occlusions, often excluded from clinical trials of acute therapy and secondary prevention. However, patients with a lacunar stroke benefit from early diagnosis, reperfusion therapy, and secondary prevention measures. In addition, there are new developments in the knowledge of this entity that suggest potential benefits of ...
Pathophysiology of Lacunar Stroke: History's Mysteries and Modern Interpretations
Journal of Stroke and Cerebrovascular Diseases, 2019
Since the term "lacune" was adopted in the 1800s to describe infarctions from cerebral small vessels, their underlying pathophysiological basis remained obscure until the 1960s when Charles Miller Fisher performed several autopsy studies of stroke patients. He observed that the vessels displayed segmental arteriolar disorganization that was associated with vessel enlargement, hemorrhage, and fibrinoid deposition. He coined the term "lipohyalinosis" to describe the microvascular mechanism that engenders small subcortical infarcts in the absence of a compelling embolic source. Since Fisher's early descriptions of lipohyalinosis and lacunar stroke (LS), there have been many advancements in the understanding of this disease process. Herein, we review lipohyalinosis as it relates to modern concepts of cerebral small vessel disease (cSVD). We discuss clinical classifications of LS as well as radiographic definitions based on modern neuroimaging techniques. We provide a broad and comprehensive overview of LS pathophysiology both at the vessel and parenchymal levels. We also comment on the role of biomarkers, the possibility of systemic disease processes, and advancements in the genetics of cSVD. Lastly, we assess preclinical models that can aid in studying LS disease pathogenesis. Enhanced understanding of this highly prevalent disease will allow for the identification of novel therapeutic targets capable of mitigating disease sequelae.