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Brain Advance Access originally published online on July 14, 2006
Brain 2006 129(9):2375-2383; doi:10.1093/brain/awl177
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© The Author (2006). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Blood pressure and haemoglobin A1c are associated with microhaemorrhage in CADASIL: a two-centre cohort study

Anand Viswanathan1,3, Jean-Pierre Guichard2, Andreas Gschwendtner4, Frederique Buffon1, Rodica Cumurcuic1, Carole Boutron1, Eric Vicaut1, Markus Holtmannspötter5, Chahin Pachai6, Marie-Germaine Bousser1, Martin Dichgans4 and Hugues Chabriat1

1 Department of Neurology, CHU Lariboisière Assistance Publique des Hôpitaux de Paris, Paris, France 2 Department of Neuroradiology, CHU Lariboisière Assistance Publique des Hôpitaux de Paris, Paris, France 3 Department of Neurology and Clinical Trials Unit, Massachusetts General Hospital and Harvard Medical School Boston, MA, USA 4 Department of Neurology, Klinikum Grosshadern Ludwig-Maximilians-University, Munich, Germany 5 Department of Neuroradiology, Klinikum Grosshadern, Ludwig-Maximilians-University Munich, Germany 6 THERALYS Lyon, France

Correspondence to: Prof. Hugues Chabriat, Service de Neurologie, Hôpital Lariboisiere, 2 rue Ambroise Paré, 75010 Paris, France E-mail: hugues.chabriat{at}lrb.ap-hop-paris.fr

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL) is a hereditary arteriopathy caused by mutations of the Notch3 gene. The risk factors for cerebral microhaemorrhages (CM), their relationship to other MRI lesions in the disease and their potential clinical impact have not been previously defined. Our purpose was to examine the frequency, number and location of microhaemorrhages in a multicentre cohort study, defining predisposing factors and associated radiographic markers in CADASIL patients. We collected clinical data from 147 consecutive patients enrolled in an ongoing prospective cohort study. Degree of neurological disability and cognitive impairment were assessed by standardized scales. T1-weighted, FLAIR and T2*-weighted gradient-echo (GE) MRI sequences were performed. Volume and location of lacunar infarcts and white matter hyperintensity (WMH) were assessed. Number and location of CM were recorded. CM were present in 35% patients, most commonly occurring in the thalamus, brainstem and basal ganglia. The location of CM qualitatively differed from areas of lacunar infarction and WMH. There was a significant association between the presence of CM and a history of hypertension (P = 0.005), systolic blood pressure (SBP) (P = 0.014), haemoglobin A1c (HbA1c) (P = 0.004) and the volume of lacunar infarcts (P = 0.010) and WMHs (P = 0.046). The number of CM was independently associated with SBP (P = 0.005), the diagnosis of hypertension (P = 0.0004), volume of WMH (P = 0.0005) and lacunar infarcts (P = 0.004). In contrast, no association was found between blood pressure or HbA1c and the load of WMH or lacunar infarcts. The presence of CM was independently associated with increased modified Rankin scores. CM are independently associated with blood pressure and HbA1c as well as with lacunar infarct and WMH volume in CADASIL. Both the vascular risk factors and regional distribution of CM appear distinct from those associated with other MRI markers, suggesting a distinct pathological process. These lesions have a potential clinical impact in CADASIL. These findings further suggest that modulation of blood pressure and glucose levels might influence the course of the disease.

Key Words: CADASIL; cerebral microhaemorrhage; lacunes; white matter damage; haemogloblin A1c

Abbreviations: CADASIL, cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy; CI, confidence interval; CM, cerebral microhaemorrhages; DBP, diastolic blood pressure; FLAIR, fluid-attenuated inversion recovery; GE, gradient-echo; HbA1c, haemoglobin A1c; ICC, intra-cranial cavity; nLV, normalized lacunar volume; SBP, systolic blood pressure; WMH, white matter hyperintensity

Received May 8, 2006. Revised May 29, 2006. Accepted June 7, 2006.


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