22. European Stroke Conference Table 1. Correlation analyses between total burden of cSVD and cognitive function Model 1 Correlation coefficient Model 2 Correlation coefficient Memory -.333‡ -.108 Executive -.312‡ -.129 function 532 © 2013 S. Karger AG, Basel Scientific Programme Information processing speed -.438‡ -.181* Overall cog-nition -.407‡ -.178* Model 1: bivariate correlation analyses. Model 2: Correlation analyses with adjustment for age and sex. * p<.05 ‡ p<.001 Figure 1. Mean Z-scores on each of the cognitive domains, stratified by cSVD category cSVD = cerebral small vessel disease 461 Small vessel stroke and white matter disease Cerebral hemorrhage in CADASIL: rare or unrecognized? I. Donnini1, V. Rinnoci2, S. Nannucci3, R. Valenti4, S. Bianchi5, F. Pescini6, D. Inzitari7, L. Panto-ni8 Department of Neurological and Psychiatric Sciences, University of Florence, Florence, IT-ALY1, Department of Neurological and Psychiatric Sciences, University of Florence, Florence, ITALY2, Department of Neurological and Psychiatric Sciences, University of Florence, Florence, ITALY3, Department of Neurological and Psychiatric Sciences, University of Florence, Florence, IT-ALY4, Neurometabolic Unit, Institute of Neurological Sciences, University of Siena, Siena, ITALY5, Department of Neurological and Psychiatric Sciences, University of Florence, Florence, ITALY6, Department of Neurological and Psychiatric Sciences, University of Florence, Florence, ITALY7, Department of Neurological and Psychiatric Sciences, University of Florence, Florence, ITALY8 Background: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoenceph-alopathy (CADASIL) is an inherited cerebral small vessel disease, clinically characterized by the occurrence of migraine, recurrent transient ischemic attacks (TIA) or strokes, cognitive decline and psychiatric disorders. In CADASIL, strokes are typically ischemic, while hemorrhagic events have been described only sporadically. However cerebral microbleeds (MBs), a predictor of increased risk of intracerebral hemorrhage (ICH), have been found in 31-69% of CADASIL patients. Methods: We describe three CADASIL patients who developed an ICH and one patient with a sub-arachnoid hemorrhage (SAH). Results: Out of a series of 60 CADASIL patients, three developed a thalamo-capsular hemorrhage (two males, age at onset: 54, 67, 77); one man had a recurrent hemispheric cerebellar hemorrhage. Another patient experienced an interpeduncolar cistern SAH when he was 39-year-old. None of these patients was receiving antiplatelet, anticoagulant or statins therapy at the time of hemorrhage but all were hypertensive. Analysis of NOTCH3 gene revealed mutations responsible for CADASIL (exons 14, 22 in two patients presenting the same c.3691C>T mutation, and 24). MBs were present on MRI in all these patients. Conclusions: ICH can occur in CADASIL as in sporadic small vessel diseases and this finding fur-ther expands the phenotype of the disease. This genetic diagnosis should probably be considered also in patients with ICH. These data bear potential implications in terms of better control of risk factors, particularly hypertension, and raise relevant questions in terms of use of antiplatelet in this disease.
Karger_ESC London_2013
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