Relevant bibliographies by topics / Lacunar infarction

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  2. Dissertations / Theses
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Academic literature on the topic 'Lacunar infarction'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 January 2023

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Journal articles on the topic "Lacunar infarction"

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Feng, Chao, Yu Xu, Ting Hua, Xue-Yuan Liu, and Min Fang. "Irregularly shaped lacunar infarction: risk factors and clinical significance." Arquivos de Neuro-Psiquiatria 71, no. 10 (October 2013): 769–73. http://dx.doi.org/10.1590/0004-282x20130119.

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Objective Our study focused on acute lacunar infarct shapes to explore the risk factors and clinical significance of irregularly shaped lacunar infarctions. Methods Based on the shape of their acute lacunar infarct, patients (n=204) were classified into the “regular” group or “irregular” group. The characteristics of the lacunar infarction were compared between the regular and irregular groups, between patients with and without neurological deterioration, and between patients with different modified Rankin scale (mRS) scores. The risk factors for irregularly shaped lacunar infarctions, neurological deterioration, and high mRS scores were identified. Results Blood pressure variability (BPV) was an independent risk factor for irregularly shaped lacunar infarction. Infarction size, prevalence of advanced leukoaraiosis, and irregularly shaped lacunar infarcts were independent risk factors for higher mRS scores. Conclusions The irregularly shaped lacunar infarcts were correlated with BPV. Irregularly shaped lacunar infarctions and leukoaraiosis may be associated with unfavorable clinical outcomes.
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Futrell, Nancy. "Lacunar Infarction." Stroke 35, no. 7 (July 2004): 1778–79. http://dx.doi.org/10.1161/01.str.0000131930.41057.48.

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Norrving, Bo. "Lacunar Infarction." Stroke 35, no. 7 (July 2004): 1779–80. http://dx.doi.org/10.1161/01.str.0000131931.84333.c0.

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Lammie, G. A., F. Brannan, and J. M. Wardlaw. "Incomplete lacunar infarction (Type I b lacunes)." Acta Neuropathologica 96, no. 2 (August 3, 1998): 163–71. http://dx.doi.org/10.1007/s004010050877.

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Kondo, Takeshi, and Kazuhiko Terada. "Strategic lacunar infarction." Medical Journal of Australia 206, no. 8 (May 2017): 340. http://dx.doi.org/10.5694/mja16.01323.

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Horowitz, D. R., S. Tuhrim, J. M. Weinberger, and S. H. Rudolph. "Mechanisms in lacunar infarction." Stroke 23, no. 3 (March 1992): 325–27. http://dx.doi.org/10.1161/01.str.23.3.325.

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Petty, George W., Douglas R. Labar, Bruce J. Fisch, Timothy A. Pedley, J. P. Mohr, and Alexander Khandji. "Electroencephalography in lacunar infarction." Journal of the Neurological Sciences 134, no. 1-2 (December 1995): 47–50. http://dx.doi.org/10.1016/0022-510x(95)00198-5.

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Potter, Gillian M., Fergus N. Doubal, Caroline A. Jackson, Francesca M. Chappell, Cathie L. Sudlow, Martin S. Dennis, and Joanna M. Wardlaw. "Counting Cavitating Lacunes Underestimates the Burden of Lacunar Infarction." Stroke 41, no. 2 (February 2010): 267–72. http://dx.doi.org/10.1161/strokeaha.109.566307.

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Oishi, Minoru, Yoko Mochizuki, and Toshiaki Takasu. "Blood Flow Differences Between Leuko-araiosis with and without Lacunar Infarction." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 25, no. 1 (February 1998): 70–75. http://dx.doi.org/10.1017/s0317167100033527.

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ABSTRACT:Background:The present study was designed to find the differences in regional cerebral blood flow and cerebrovascular acetazolamide reactivity between leuko-araiosis with and without lacunar infarction.Methods:Fifteen cases of leuko-araiosis with lacunar infarction, 15 cases of leuko-araiosis without lacunar infarction and 15 age-matched controls in which leuko-araiosis and cerebrovascular diseases are absent (control group) were studied. The regional cerebral blood flow was measured using the stable xenon computed tomography method before and 20 minutes after intravenous injection of 17 mg/kg acetazolamide.Results:The blood flows in the leuko-araiosis area and the lacunar area were significantly lower than the blood flow in the cerebral white matter. The blood flows in the cerebral cortex and the cerebral white matter were significantly lower in the leuko-araiosis with lacunar infarction group than in the leuko-araiosis without lacunar infarction group and the control group. The cerebrovascular acetazolamide reactivity in the leuko-araiosis area and the lacunar area was significantly lower than that in the cerebral white matter. The cerebrovascular acetazolamide reactivity in the cerebral cortex and the cerebral white matter was significantly lower in the leuko-araiosis with lacunar infarction group than in the leuko-araiosis without lacunar infarction group and the control group.Conclusions:The degree of arteriolosclerosis is considered to be more severe and the rate of association of hypertension was higher in leuko-araiosis with lacunar infarction than in leuko-araiosis without lacunar infarction.
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Koch, S., M. S. McClendon, and R. Bhatia. "Imaging evolution of acute lacunar infarction: Leukoariosis or lacune?" Neurology 77, no. 11 (August 31, 2011): 1091–95. http://dx.doi.org/10.1212/wnl.0b013e31822e1470.

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Dissertations / Theses on the topic "Lacunar infarction"

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Jackson, Caroline Anne. "Epidemiology of ischaemic stroke subtypes : do differences in epidemiology provide evidence for a distinct lacunar arterial pathology?" Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4307.

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Background Lacunar ischaemic stroke accounts for around one quarter of all strokes, and is presumed to result from the occlusion of a single perforating artery supplying the deep subcortical areas of the brain. The underlying arterial pathology is poorly understood, but is thought to differ from the atherothrombotic processes that occlude larger intra- and extracranial arteries causing most other ischaemic stroke subtypes. Progress in understanding the aetiology of lacunar stroke has been limited by the lack of informative autopsy studies, and the difficulties in studying small blood vessels using brain imaging. One alternative approach is to compare the epidemiology of ischaemic stroke subtypes, since differences in the epidemiology may reflect and inform about different underlying pathologies. Methods I performed two systematic literature reviews to identify studies presenting data on (1) the risk factors for, and (2) the outcome of, different ischaemic stroke subtypes. I extracted relevant data from included studies and performed a series of meta-analyses comparing risk factor profiles, and risks of death, recurrent stroke and myocardial infarction (MI) in patients with lacunar versus non-lacunar ischaemic stroke. To address some of the unanswered questions and controversies surrounding the causes of ischaemic stroke we set up the Edinburgh Stroke Study (ESS), which I co-ordinated. We recruited patients with stroke and transient ischaemic attack seen at our hospital between 2002 and 2005, and followed them for 1-4 years for death, recurrent stroke and MI. To overcome the methodological limitations of the studies included in my reviews and of my meta-analyses, I carried out a large collaborative individual patient data analysis in which I combined data from five stroke registries - including the ESS - that had used similar robust methodology, and performed a series of analyses comparing the risk factor profiles of patients with lacunar versus nonlacunar ischaemic stroke. In an updated meta-analysis, I combined this data with existing published studies that had used an unbiased method of classifying ischaemic stroke subtypes. Using the ESS data, I compared the risks of recurrent stroke and MI, and patterns of recurrent stroke subtypes in patients with lacunar versus nonlacunar stroke. Results In my systematic review of risk factors I found evidence of classification bias in many studies, where systematic error was introduced through the use of classification methods that included risk factors in the definitions of stroke subtypes. This led to overestimation of some risk factor-stroke subtype associations and, in particular, to apparently stronger associations between hypertension and diabetes and lacunar compared with non-lacunar ischaemic stroke. When I included only unbiased studies, I found a significantly reduced prevalence of atrial fibrillation (AF) and severe carotid stenosis and a trend towards a reduced prevalence of ischaemic heart disease (IHD) in lacunar patients. I found a very slight excess of hypertension among lacunar patients, but no difference in the prevalence of diabetes, or any other risk factor studied. In my collaborative individual patient data analysis, I confirmed a significantly lower prevalence of severe carotid stenosis, AF and previous IHD in patients with lacunar ischaemic stroke, but found no difference in the prevalence of hypertension, diabetes, or any other risk factor studied, even after adjusting for confounding factors. These results were largely confirmed in my updated metaanalysis, although there was a slight excess of hypertension among lacunar compared with non-lacunar ischaemic strokes. In my systematic review of outcome after lacunar versus non-lacunar ischaemic stroke, I found a lower risk of death following lacunar compared with non-lacunar stroke which attenuated but persisted long-term; a higher recurrent stroke risk in non-lacunar patients during the first month only; and limited data on recurrent stroke subtypes suggesting that ischaemic stroke subtypes may breed true to type. Data on MI risk were extremely sparse. My analyses of data from the ESS showed no difference overall in risk of recurrent stroke between patients with lacunar versus non-lacunar ischaemic stroke, but some evidence for a lower very early recurrence risk among lacunar patients. There was evidence that recurrent stroke subtypes breed true, since patients with a lacunar stroke at baseline were much more likely to have a lacunar than a non-lacunar recurrence. We identified five times as many MI events following stroke than have been previously reported in the published literature, and found a non-significantly reduced risk of MI in patients with lacunar compared with non-lacunar ischaemic stroke. Conclusions My comparisons of the epidemiology of lacunar versus non-lacunar ischaemic stroke subtypes revealed differences in the risk factor profiles and risks of recurrent stroke and myocardial infarction which suggest that a distinct, nonatherothrombotic arteriopathy underlies many lacunar ischaemic strokes. My analyses of recurrent stroke subtype patterns suggest that recurrent ischaemic strokes subtypes tend to breed true, providing further support for a distinct lacunar arteriopathy. Contrary to widespread belief, hypertension and diabetes do not appear to be more important in the aetiology of lacunar stroke than in other types of ischaemic stroke. These findings support other lines of evidence for a distinct lacunar arteriopathy, and highlight the need for further research into the aetiology of lacunar ischaemic stroke.
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WADA, KENTARO, TOMOYUKI NODA, KENICHI HATTORI, HIDEKI MAKI, AKIRA KITO, and HIROFUMI OYAMA. "Atherothrombotic Lesion of the Middle Cerebral Artery: Report of 21 Cases with Stenotic and Obstructive Lesions." Nagoya University School of Medicine, 2013. http://hdl.handle.net/2237/17600.

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Rogers, Heather L. "Cognitive function and emotional status of middle-aged chinese hypertensive patients without detectable white matter brain lesions or lacunar infarctions /." Download the thesis in PDF, 2006. http://www.lrc.usuhs.mil/dissertations/pdf/Rogers2006.pdf.

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Lam, Ada Karman. "Endothelial function & genetic polymorphisms in cerebral small vessel disease: a study investigating the relationship between endothelial function, genetic polymorphisms and cerebral small vessel disease." Thesis, 2010. http://hdl.handle.net/2440/65210.

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Background: The pathogenesis of cerebral small vessel disease (SVD), encompassing lacunar infarction (LI) and leukoaraiosis (LA), is heterogeneous, with impaired endothelial function (EF) and altered fibrinolysis proposed as important contributors. Genetic factors are involved and may exert their influence via the above mechanisms. The aim of this study was to explore the relationship between EF and SVD, and to examine the role of candidate polymorphisms in both EF and SVD. Methods: The study cohort consisted of patients who had undergone a brain magnetic resonance image (MRI) scan for non-vascular indications. Vascular risk factors were collected by interviewing participants. SVD was classified using a modified Fazekas rating scale, where SVD burden was divided into three categories: absent/mild, moderate and severe. LI was graded separately. EF was assessed using applanation tonometry (ApT) and the radial pulsewave. A global EF score that accounts for both endothelium-dependant and –independent vasodilation was used as the index for comparison. A higher global EF score indicated better EF. Participants were genotyped using the sequence-specific polymerase chain reaction (PCR-SS) for eight candidate polymorphisms chosen based on biological plausibility and/or previous study evidence: interleukin-6 (IL-6) -174 G/C, NADPH oxidase p22 phox 242 C/T, tissue plasminogen activator (tPA) 20324 C/T, tPA -4360 G/C, tPA -7351 C/T, endothelial nitric oxide synthase (eNOS) -786 T/C, endothelin-1 (ET-1) 138 D/I and paraoxonase-1 (PON1) -107 C/T. Statistical analyses were performed using Intercooled Stata 9.2, GraphPad Prism and the SNPstats. Regression models were adjusted for the appropriate variables. Results: A total of 132 participants were assessed. All participants were genotyped and 84 of these 132 participants also had their EF assessed using ApT, but only 72 participants were successful. Participants were graded separately for LI and LA. LA controls (n=119) were defined as participants with absent/mild LA, and LA cases (n=13) were participants with moderate or severe LA. LI controls (n=126) were participants without a radiologically defined LI and LI cases (n=6) were participants with radiologically defined LI. The results of the study can be summarised as follows: 1. there was no significant difference between the EF of cases and controls. Subgroup analyses showed that the risk of LA decreased as the global EF values increased after adjusting for confounding influences, but the relationship was not significant (p=0.23); 2. there were no significant differences in EF between the genotypes of the eight candidate polymorphisms, except for the tPA 20324 C/T, where the TT genotype was associated with higher EF compared to the CC/CT genotypes (p=0.02); 3. the tPA 20324 TT genotype was significantly associated with an increased risk of LI compared to the CC/CT genotypes (p=0.03), although the association is under powered. No other significant associations were found. Although the intent was to achieve a pre-determined sample size, the methodology, and in particular the exclusion criteria, restricted recruitment and consequently the study was under powered to achieve its goals. The study could therefore be considered a pilot study and any conclusions forthwith require validation in a larger sample. Conclusion: The tPA 20324 TT genotype was significantly associated with LI, while also being significantly associated with better EF. This result may be a Type I error reflective of the small sample size. However, the result does support the hypothesis that impaired fibrinolysis has an important pathogenic role in LI. This study does not support impaired EF as a significant pathogenic contributor to SVD.
Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2010
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Books on the topic "Lacunar infarction"

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A, Donnan G., ed. Lacunar and other subcortical infarctions. Oxford: Oxford University Press, 1995.

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A, Donnan G., ed. Lacuna and other subcortical infarctions. New York: Oxford University Press, 1995.

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Book chapters on the topic "Lacunar infarction"

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Roth, Elliot J. "Lacunar Infarction." In Encyclopedia of Clinical Neuropsychology, 1947–48. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_2188.

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Roth, Elliot J. "Lacunar Infarction." In Encyclopedia of Clinical Neuropsychology, 1–2. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-56782-2_2188-2.

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Roth, Elliot J. "Lacunar Infarction." In Encyclopedia of Clinical Neuropsychology, 1421. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_2188.

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Liou, Chia-Wei, Tsu-Kung Lin, Feng-Mei Huang, Tzu-Ling Chen, Cheng-Feng Lee, Yao-Chung Chuang, Teng-Yeow Tan, Ku-Chou Chang, and Yau-Huei Wei. "Association of the Mitochondrial DNA 16189 T to C Variant with Lacunar Cerebral Infarction." In Mitochondrial Pathogenesis, 317–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-41088-2_31.

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Kalvach, P., R. Schickerová, and J. Vymazal. "Cerebral lacunes: an image of interterritorial infarction." In Proceedings of the XIV Symposium Neuroradiologicum, 379–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-49329-4_134.

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"Lacunar Infarction." In Imaging in Neurology, 101. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-323-44781-2.50075-9.

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"Lacunar Infarction." In Diagnostic Imaging: Brain, 368–71. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-323-37754-6.50112-3.

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Kase, Carlos S., and Conrado J. Estol. "Lacunar Infarction." In Office Practice of Neurology, 309–14. Elsevier, 2003. http://dx.doi.org/10.1016/b0-44-306557-8/50034-4.

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Caplan, Louis R. "Neurological Examination of the Stuporous Patient, Lacunar Infarction, Intracerebral Hemorrhage, and Aneurysmal Subarachnoid Hemorrhage." In C. Miller Fisher, edited by Louis R. Caplan, 170–91. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190603656.003.0010.

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Abstract: This chapter describes some of Fisher’s major contributions in neurology, stroke, and cerebrovascular disease. The main areas are the neurological examination, especially in patients with decreased consciousness; the pathology of penetrating artery disease and lacunar infarction and the associated clinical findings; the pathology and clinical features of intracerebral hemorrhage and description of the findings in cerebellar hemorrhage; and the presence and clinical features of delayed cerebral infarction and arterial vasoconstriction in patients with aneurysmal subarachnoid hemorrhage. His contributions were often made over time. He often worked on different areas of interest concurrently. When he prepared a list in 1998 of his own contributions for a Canadian Medical Hall of Fame biographer, he listed 101 separate contributions.
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Caplan, Louis R. "Montreal, 1950–1954." In C. Miller Fisher, edited by Louis R. Caplan, 106–30. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190603656.003.0007.

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Abstract: This chapter describes Fisher’s career in Montreal (1950–1954) and his ultimate transfer to Boston. His family life, studies, accomplishments, and writings during this period are also described. Highlighted are his discoveries about carotid artery disease, transient loss of vision, transient episodes of brain ischemia, lacunar brain infarction and its mechanisms, brain embolism, and the distribution of atherosclerosis within the arteries that supply the brain. While in Montreal, Fisher became a productive researcher. His work on carotid artery disease and temporary episodes of eye and brain ischemia gained him widespread recognition. However, he eventually decided that the future of his stroke work was far brighter in Boston than if he stayed in Montreal, and so he eventually decided to return to Boston.
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Conference papers on the topic "Lacunar infarction"

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Liu, Xin, Wengang Yin, and Luping Song. "A acalculia case of mathematical concepts deficits from multiple lacunar infarction." In 2017 10th International Congress on Image and Signal Processing, BioMedical Engineering and Informatics (CISP-BMEI). IEEE, 2017. http://dx.doi.org/10.1109/cisp-bmei.2017.8302084.

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