White matter lesions and lacunar infarcts are differentially associated with brain atrophy: The smart-MR study

White matter lesions and lacunar infarcts are differentially associated with brain atrophy: The smart-MR study

308 Abstracts / Journal of the Neurological Sciences 283 (2009) 240–320 Hispanic cohort in the United States and to compare the predictive value of ...

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308

Abstracts / Journal of the Neurological Sciences 283 (2009) 240–320

Hispanic cohort in the United States and to compare the predictive value of the MeSy to diabetes and hyperinsulinemia. Methods: We conducted cross-sectional and prospective analyses in two thousand four hundred seventy-six men and women aged 65 years and older at baseline and with data available on the metabolic syndrome and dementia diagnosis in Northern New York City. MeSy was defined by the NCEP-ATPIII and EGIR-criteria using waist, lipids, insulin, blood pressure, hypertension and diabetes. Dementia was diagnosed using DSM-IV and NINCDS criteria and classified as AD or dementia associated with stroke (DAS). Results: In 2476 individuals, no association was found between MeSy and prevalent dementia. After 4.4 years of follow-up, 236 individuals of the 1833 without prevalent dementia developed dementia (147 AD, 73 DAS, 16 other). No relation was found between MeSy and incident dementia. Of the separate risk factors of the MeSy, diabetes and hyperinsulinemia were associated with an increased risk of incident AD (HR; 95%CI respectively 1.4; 1.0–2.1 and 1.4; 0.9–2.7) and DAS (HR; 95%CI respectively 1.9; 1.1–3.1 and 2.3; 1.1–4.7). Conclusions: The MeSy is not associated with an increased risk of dementia in a multiethnic elderly cohort, but diabetes and hyperinsulinemia were. Our results suggest that in the elderly examining diabetes and hyperinsulinemia separately may be preferable to using the metabolic syndrome as a risk factor. doi:10.1016/j.jns.2009.02.257

secondary to small vessel disease, and usually linked to common vascular RF. We set to analyze RF in our population of patients with ischemic WML. WML has not been studied systematically in Serbia before. Methods: We conducted a prospective study enrolling consecutive patients with ischemic cerebral WML admitted to our hospital in a 4-year period. Analysis comprised demographic data, vascular RF, score on modified Rankin Scale, results of neuropsychological testing, Hamilton depression scale score, and total score on the Age Related White Matter Changes Scale. Fifty patients with first lacunar stroke comprised control group. Both groups were age and sex matched. Results: A total of 200 patients with WML were included in the study, age ranged from 35 to 82 years, mean age 62 ± 11 years, 55% male. RF comparison between groups showed that most frequent vascular RF in the WML group were hypertension (82.5%), dyslipidaemia (79.0%) and previous stroke (57.5%). Hypertension increased risk for WML 2.2 times (OR 2.2; 95% CI 1.1–4.7, p = 0.038), dyslipidemia 3 times (OR 3.0; 95% CI 1.5–6.0, p = 0.002), and history of previous stroke over 30 times (OR 32.5; 95% CI 7.4–198.8, p < 0.0001). In multivariate analysis, dyslipidemia (OR 2.5, p = 0.015) and previous stroke (OR 30.1, p < 0.0001) remained independent predictors of ischemic WML. Conclusions: In our dataset, dyslipidemia and history of previous stroke were strong and independent predictors of ischemic WML. doi:10.1016/j.jns.2009.02.259

Study about risk factors for cognitive decline in patients with ischemic stroke V. Tudorica, C. Zaharia, D. Stanca, D. Pirscoveanu Clinic of Neurology, Clinical Hospital of Neuropsychiatry, Craiova, Dolj, Romania Objective: The aim of the study was to evaluate the factors involved in developing cognitive decline after ischemic stroke. Material and methods: We studied 375 patients with ischemic stroke admitted in The Clinic of Neurology Craiova during the year 2005. The study group was composed of 174 men and 201 women, aged between 44 and 85 years. The patients were divided in 4 groups: group A aged between 41 and 50 years, group B aged between 51 and 60 years, group C aged between 61 and 70 years and group D aged above 71 years. 293 patients had ischemic stroke in the carotid artery territory and 82 in the vertebro-basilar artery territory. Each patient was evaluated concerning the risk factors of stroke, the treatment for these factors and, where was possible, we received information about the preexistent mental status. We performed The Mini Mental Status Examination, The Clock Drawing Test and Cognitive Capacity Screening Examination for each patient. These evaluations were realized 3 months after stroke and than 1 year later. The results were analyzed by Student’s Test. Results: The cognitive decline was significant statistically 1 year after the stroke in 22.5% of patients. The women were more affected but not in a statistically significant manner in comparison with men. The cognitive decline was statistically significant higher in group D with more than 3 risk factors for stroke and with multiple strokes in the carotid artery territory. Conclusion: Some factors can be taken into consideration as predictors for cognitive decline after ischemic stroke. doi:10.1016/j.jns.2009.02.258

Risk factors for ischemic white matter lesions D.M. Pavlovic, A.M. Pavlovic, T. Pekmezovic, J. Zidverc-Trajkovic, Z. Jovanovic, M. Mijajlovic, G. Tomic, A. Radojicic, N. Sternic Institute of Neurology, Clinical Center of Serbia, Belgrade, Serbia Background and aims: Cerebral WML are frequently detected on MRI scans in healthy elderly individuals, patients with vascular risk factors (RF), stroke survivors, and patients with dementia. It is believed that WML are

White matter lesions and lacunar infarcts are differentially associated with brain atrophy: The smart-MR study A.P. Appelmana,b, Y. van der Graafb, A.M. Tiehuisa, K.L. Vinckenc, T.D. Witkampa, W.P. Malia, M.I. Geerlingsb a Department of Radiology, University Medical Center Utrecht, Utrecht, The Netherlands b Julius Center For Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands c Image Sciences Institute, University Medical Center Utrecht, Utrecht, The Netherlands Background and aims: Cerebral small-vessel disease (CSVD) may be involved in the pathogenesis of brain atrophy. However, the independent impact of white matter lesions (WML) and lacunar infarcts (LI) on brain atrophy is unknown. We investigated the independent association of WML and LI with brain atrophy. Methods: Within the SMART-MR study, a prospective cohort study among patients with manifest arterial disease, cross-sectional analyses were performed in 992 patients (mean age 58 ± 10 years, 79% male) without cortical infarctions. Brain segmentation was used to quantify volumes of brain tissue, cerebrospinal fluid and WML. Total brain volume, ventricle volume and cortical gray matter volume were divided by intracranial volume to obtain brain parenchymal fraction (BPF), ventricle fraction (VF) and cortical gray matter fraction (GMF). Lower BPF indicates more global brain atrophy, higher VF indicates more subcortical atrophy and lower GMF indicates more cortical atrophy. Location and number of infarcts were rated visually. Results: Mean BPF was 79.2 ± 2.9%, mean VF was 2.03 ± 0.96% and mean GMF was 36.5 ± 3.3%. Linear regression analyses, adjusted for age, sex, vascular risk factors, intima-media thickness and lacunar infarcts, showed that in patients with moderate to severe WML (upper quartile) BPF was lower (− 0.62%; 95%CI − 1.04 to − 0.19%), VF was higher (0.55%; 95%CI 0.38 to 0.72%) and GMF was lower (− 1.60%; 95%CI − 2.19 to − 1.01%) than in patients with few WML (lower quartile). Presence of LI was associated with lower BPF (− 0.57%; 95%CI − 1.00 to − 0.14%) and higher VF (0.30%; 95%CI 0.12 to 0.48%), but not with GMF, independent of WML and other potential confounders. Conclusions: In patients with manifest arterial disease, WML are related to all measures of brain atrophy, independent of the presence of LI and vascular risk factors. LI are independently related to more global and subcortical atrophy, but not to cortical atrophy. doi:10.1016/j.jns.2009.02.260