Regular ArticleAdmission markers predict lacunar and non-lacunar stroke in young patients
Introduction
Stroke in young adults is an important cause of lifelong morbidity, thus it is important to focus on the prognosis of young cerebral infarction patients. In arterial thrombosis at young age, traditional risk factors such as gender, smoking, diabetes mellitus, obesity and hypercholesterolemia do not fully explain the cerebrovascular risk [1], [2], [3], [4].
The three most common etiology of cerebral infarction are large-vessel atherosclerosis, small vessel disease and cardiac embolism [5], [6]. Histopathologic study disclosed that small vessel disease causes subcortical infarctions < 1.5 cm in diameter (lacunar stroke) [7]. None-lacunar infarctions comprising subcortical infarctions and brainstem infarctions ≥ 1.5 cm with or without involvement of the cortex and pure cortical infarctions tend to be associated with large-vessel atherosclerosis and cardiac embolism [8]. These have included observational studies comparing the risk factor profiles of patients with lacunar versus non-lacunar infarction, since differences might suggest distinct arterial pathologies.
Clinically, we found it is very subjective to distinguish clearly lacunar infarction or non-lacunar cerebral infarction in young patients only through clinical symptoms and signs in contrast to laboratory and radiological indicators. Brain CT imaging studies are often unable to identify existing lesions when they are performed on young patients within the early onset of disease (most of them within 24 hours). Therefore, we often miss the best time to take appropriate treatment for young patients.
In the study, we conducted a retrospective study on a series of young patients with cerebral infarction and compared a group of definite lacunar infarcts with another group of nonlacunar infarcts by analysing the distribution of vascular risk factors and several clinical/instrumental variables. The aim of this study was to explore some possible admission indicators related to subsequent lacunar or non-lacunar strokes.
Section snippets
Methods
All patients were 18 to 45 years old and first-ever cerebral infarction during 2001–2010. Consecutive patients come from the Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Chinese mainland. Our institution is the biggest hospital that covers an urban area of approximately 2500 000 individuals who are all Chinese. To avoid misdiagnosis of lacunar stroke in patients recovering from more extensive clinical deficits, we included only patients visited within two days of their
Statistical Analyses
Statistical analyses were performed with the χ2 test for binary and categorical data and the Mann–Whitney U test for continuous variables. Data are presented as means ± standard deviations.
Multivariate analysis was performed by binary logistic regression analysis, which allows adjustment for confounding factors. All variables have an inclusion criterion of P < 0.10 that were at least weakly associated with stroke severity. A binary logistic regression model that included age at onset, diabetes
Results
Of the 626 patients with acute stroke, lacunar strokes were found in 262 patients and non-lacunar strokes were found in the 364 patients. Baseline characteristics of the patients are given in Table 1, the mean age at onset among lacunar strokes was significantly older than non-lacunar strokes (P < 0.001), non-lacunar strokes were characterized by the serious admission and discharge neurological impairment (respectively NIHSS = 8.5 ± 7.2, 4.7 ± 5.9) (P < 0.001). Hypertension, hyperlipidemia, atrial
Discussions
Within the frame of a young patients-based study, we have confirmed that some differences between lacunar and non-lacunar strokes. We have also shown that there are some indicators to relate to which stroke patients will most likely to develop a lacunar or non-lacunar. Unlike several previous studies [11], [12], we did not try to subdivide the non-lacunar strokes into ardioembolic and therothrombotic according to their pathogenesis, since this distinction is often difficult or even impossible,
Funding/Support
This study was supported by grant Guangdong Provincial Science and Technology Program, grant 2009B030801363, and supported by Science and technology projects in Guangdong Province, grant 2010B031600143.
Conflict of interest statement
Competing interests: The authors declare that they have no competing interests.
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2018, Clinical Neurology and NeurosurgeryCitation Excerpt :The cause of the lacunar infarcts has been much debated and the pathology underlying lacunar infarcts remains undetermined [4]. Besides the intrinsic cerebral small arteriolar abnormality, other suggestions including intracranial large artery atheromatous stenosis [5,6], carotid stenosis [7], and moyamoya disease [8], and emboli from large arteries or heart [9,10], account for 10–15% of lacunar strokes [11]. Moyamoya disease is a progressive arteriopathy characterized by steno-occlusive changes of the distal internal carotid artery, with abnormal vascular networks (the moyamoya vessels) formation at the base of the brain [12,13].
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Bin Zhang and WeiZhi Zhang are the co-first author.