Subcortical gray matter N-acetylaspartate reduction in two cases of vascular dementia Douraied Ben Salem a, *, Paul Michael Walker b , Guy-Victor Osseby c , Denis Krause ´ a , Maurice Giroud c , Franc ¸ois Brunotte b a Department of Neuroradiology, Dijon University Hospital, 3 rue du faubourg raines, 21033 Dijon Cedex, France b Department of MR Imaging and Spectroscopy, Dijon University Hospital, Dijon Cedex, France c Department of Neurology, Dijon University Hospital, Dijon Cedex, France Received 4 April 2002; accepted 10 May 2002 Abstract Many of the previous studies of vascular dementia using proton magnetic resonance (MR) spectroscopy had been carried out on white matter. However, no proton spectroscopic data of the subcortical gray matter are available in such disease. We report two cases suffering from vascular dementia, with an unilateral N-acetylaspartate (NAA) decrease on subcortical gray matter. This significant reduction in NAA ratios was associated with an increase of choline on the ipsilateral centrum semiovale. We discuss the pathophysiology of these cases. D 2002 Elsevier Science Inc. All rights reserved. Keywords: Vascular dementia; Brain; Gray matter; Magnetic resonance spectroscopy 1. Introduction Small-vessel disease is a subtype of vascular dementia, related to hypertension and arteriosclerosis [1]. Lesions, caused by deep penetrating nonbranching arteriole occlu- sion or narrowing, involve watershed areas of subcortical gray or white matter [2,3]. Proton magnetic resonance spectroscopy ( 1 H-MRS) stud- ies of vascular dementia have demonstrated an unspecific decrease of N-acetylaspartate (NAA) [4–6] in subcortical white matter hyperintensities, but no proton spectroscopic data of subcortical gray matter (basal ganglia and thalami) have been published in such dementia. 2. Case reports 2.1. Case 1 A 57-year-old man had been suffering since 1997 from a small-vessel disease with dementia established on the basis of the National Institute of Neurological Disorders and Stroke – Association Internationale pour la Recherche et l’Enseignement en Neurosciences criteria [1] (NINDS/ AIREN). He was admitted to hospital on December 1999 20 h after a right transient hemiparesis. He had a history of risk factors for cardiovascular disease such as hypertension (since 1984), smoking (38 packet years), diabetes mellitus type II (treated by glibenclamide). His family had noticed over the past few months frequent unprovoked falls. On admittance, the initial neurological examination did not find the right deficit, but a right ankle clonus was noticed with a small-step gait (marche a ` petit pas) and archaic reflexes. Cognitive study showed bradyphrenia and decline in short delay memory. His blood pressure was 170/90 mm Hg under bitherapy (losartan and cicletanine), but reached 200/120 mm Hg 3 days later. Carotid Doppler-sonography did not reveal any significant stenosis. The magnetic resonance (MR) examination was carried out using a 1.5-T Magnetom Vision whole body imager (Siemens, Erlangen, Germany). Standard MR imaging of the brain included sagittal, coronal and axial T2-weighted turbo spin-echo sequence (TE = 14/85 ms, TR = 3500 ms, slice thickness 5 mm), axial fluid-attenuated inversion recovery (TE = 119 ms, TR = 7500 ms, TI = 2357 ms, slice 0899-7071/03/$ – see front matter D 2002 Elsevier Science Inc. All rights reserved. PII:S0899-7071(02)00483-7 * Corresponding author. Tel.: +33-380-293744; fax: +33-380-293866. E-mail address: douraied@lycos.fr (D. Ben Salem). Journal of Clinical Imaging 27 (2003) 14 – 17