I am seeking infromation about small vessel disease/leucoaraiosis causing cognitive impairment, without grey matter degenerative signs (tangles and plaque) or symptoms (AD,LBD, FTD), so to adscribe cognitive symptons purelly to vascular factors
Department of Stroke, Neurological Hospital, Université Lyon 1, Lyon, France.
2
Pôle Information Médicale Evaluation Recherche, Hospices Civils de Lyon, Lyon, France.
3
Department of Neuroradiology, Neurological Hospital, Université Lyon 1, 59 Bd Pinel, 69677, Bron, Lyon, France.
4
RESUVAL Stroke Network, Lyon, France.
5
Department of Neuroradiology, Neurological Hospital, Université Lyon 1, 59 Bd Pinel, 69677, Bron, Lyon, France. [email protected].
Abstract
INTRODUCTION:
Severity of vascular damage of white matter may predict hemorrhagic transformation (HT). We assess the relationship between leukoaraiosis (LA) severity and the type of hemorrhagic transformation in elderly patients treated with thrombolysis.
METHODS:
We retrospectively analyzed the clinical data and pretreatment magnetic resonance imaging (MRI) of 180 consecutive ischemic stroke patients aged over 75 years. LA severity was graded according to the Fazekas scale, and acute diffusion-weighted-imaging (DWI) lesion volumes were semi-automatically outlined. Predictors of hemorrhagic infarction (HI) and parenchymal hemorrhage (PH) were identified using logistic regression analysis and exact multinomial logistic analysis.
RESULTS:
HT occurred in 31 patients (17 %). Baseline National Institute of Health Stroke Score (NIHSS; p = 0.008), severe LA (p = 0.02), and diffusion lesion volume (p = 0.02) were predictors of HT in univariable logistic regression. Adjusted to lesion volume and baseline NIHSS score, exact multinomial logistic analysis showed that severe LA was the only independent predictor of parenchymal hemorrhage (p = 0.03).
CONCLUSION:
In elderly patients, LA severity better predicts parenchymal hemorrhage than infarct size.
KEYWORDS:
Elderly; Ischemic stroke; Leucoaraiosis; Magnetic resonance imaging; Thrombolysis
2. Association study of TREM2 polymorphism rs75932628 with leucoaraiosis or Parkinson's disease in the Han Chinese population.
Li Z, Zhong L, Gu L, Huang W, Shi X, Zhang X, An X, Lin Q, Tzeng CM.
BMJ Open. 2016 Jan 12;6(1):e009499. doi: 10.1136/bmjopen-2015-009499.
PMID:
26758262
Free PMC Article
The (2) article is freely downloadable at the following site:
We have studied microvascular changes and white matter disease in dementia since many years (and we currently do). Please have a look at Haglund M and/or Sjobeck M with Englund E from years 2002 and on. If the info is in line with what you seek, I'll be glad to provide more extensive text.
Department of Neurology, The University of Tokyo Hospital, Tokyo, Japan.
2
Center for Epidemiology and Preventive Medicine, The University of Tokyo Hospital, Tokyo, Japan.
Abstract
AIM:
To clarify whether carotid atherosclerosis and its risk factors are associated with cognitive decline.
METHODS:
We evaluated 206 individuals who visited our center for health screening. We carried out physical examinations, blood tests, intima-media thickness (IMT) measurement by carotid ultrasonography, brain magnetic resonance imaging scanning and cognitive function assessments. A total of 30 individuals, who had significant cerebrovascular lesions detected in magnetic resonance imaging scans, were excluded. To detect early cognitive decline, we defined "cognitive impairment (CI)" when a patient satisfied at least one of three criteria. These were Mini-Mental State Examination score
abstract downloaded Yesterday from Lancet Neurology
Detection, risk factors, and functional consequences of cerebral microinfarcts
Susanne J van VeluwxSusanne J van Veluw
Department of Neurology, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, Netherlands
Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA, , PhD
,Andy Y ShihxAndy Y Shih
Department of Neuroscience, Medical University of South Carolina, Charleston, SC, USA, , PhD
,Eric E SmithxEric E Smith
Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada, MD
,Christopher ChenxChristopher Chen
Memory Ageing and Cognition Centre, National University Health System, Singapore
, MD,
Prof Julie A SchneiderxJulie A Schneider
Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA, MD,
Prof Joanna M WardlawxJoanna M Wardlaw
Centre for Clinical Brain Sciences and Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK, MD
,Prof Steven M GreenbergxSteven M Greenberg
Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA, MD
,Prof Geert Jan BiesselsxGeert Jan Biessels
Department of Neurology, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, Netherlands
Correspondence to: Prof Geert Jan Biessels, Department of Neurology, Brain Center Rudolf Magnus, University Medical Center Utrecht, 3508 GA Utrecht, Netherlands
, MD Correspondence information about the author Prof Geert Jan BiesselsxGeert Jan Biessels
Department of Neurology, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, Netherlands
Correspondence
Correspondence to: Prof Geert Jan Biessels, Department of Neurology, Brain Center Rudolf Magnus, University Medical Center Utrecht, 3508 GA Utrecht, Netherlands
Cerebral microinfarcts are small lesions that are presumed to be ischaemic. Despite the small size of these lesions, affected individuals can have hundreds to thousands of cerebral microinfarcts, which cause measurable disruption to structural brain connections, and are associated with dementia that is independent of Alzheimer's disease pathology or larger infarcts (ie, lacunar infarcts, and large cortical and non-lacunar subcortical infarcts). Substantial progress has been made with regard to understanding risk factors and functional consequences of cerebral microinfarcts, partly driven by new in-vivo detection methods and the development of animal models that closely mimic multiple aspects of cerebral microinfarcts in human beings. Evidence from these advances suggests that cerebral microinfarcts can be manifestations of both small vessel and large vessel disease, that cerebral microinfarcts are independently associated with cognitive impairment, and that these lesions are likely to cause damage to brain structure and function that extends beyond their actual lesion boundaries. Criteria for the identification of cerebral microinfarcts with in-vivo MRI are provided to support further studies of the association between these lesions and cerebrovascular disease and dementia.