White matter lesions are frequently found on cerebral MRI scans of elderly people and are thought to be important in the pathogenesis of dementia. Hyper tension has been associated with the presence of white matter lesions but this has been investigated almost exclusively in cross-sectional studies. We studied prospectively the association of these lesions with the duration and treatment of hypertension. We randomly sampled 1077 subjects aged between 60 and 90 years from two prospective population-based studies. One-half of the study subjects had their blood pressure measured between 1975 and 1978 and the other half between 1990 and 1993. All subjects underwent 1.5 T MRI scanning; white matter lesions in the subcortical and periventricular regions were rated separately. Subjects with hypertension had increased rates of both types of white matter lesion. Duration of hypertension was associated with both periventricular and subcortical white matter lesions. This relationship was influenced strongly by age. For participants with >20 years of hypertension and aged between 60 and 70 years at the time of follow-up, the relative risks for subcortical and periventricular white matter lesions were 24.3 [95% confidence interval (CI) 5.1-114.8] and 15.8 (95% CI 3.4-73.5), respectively, compared with normotensive subjects. Subjects with successfully treated hypertension had only moderately increased rates of subcortical white matter lesions and periventricular white matter lesions (relative risk 3.3, 95% CI 1.3-8.4 and 2.6, 95% CI 1.0-6.8, respectively) compared with normotensive subjects. For poorly controlled hypertensives, these relative risks were 8.4 (95% CI 3.1-22.6) and 5.8 (95% CI 2.1-16.0), respectively. In conclusion, we found a relationship between long-standing hypertension and the presence of white matter lesions. Our findings are consistent with the view that effective treatment may reduce the rates of both types of white matter lesion. Adequate treatment of hypertension may therefore prevent white matter lesions and the associated cognitive decline.

Objective Formerly eclamptic women demonstrate cerebral white matter lesions (WMLs) several years following the index pregnancy. The pathophysiology is unclear and may be related to the predisposition for cerebrovascular/cardiovascular disease in such women and/or the occurrence of posterior reversible encephalopathy syndrome whilst pregnant. The aim of this study was to assess the presence and severity of WMLs and their relationship with the severity of the neurological symptoms during the index pregnancy and several current cardiovascular risk factors in formerly pre-eclamptic women.Design This was a retrospective cohort study.Setting The Neuroimaging Centre at the School for Behavioural and Cognitive Neurosciences, Groningen, the Netherlands.Population Seventy-three formerly pre-eclamptic women were matched for age (37 ± 6 years) and elapsed time since index pregnancy (5.1 ± 3.7 years) with parous control women.Methods Cerebral magnetic resonance imaging scans were performed on cases and controls. Scans were rated by a neuroradiologist blind to the patient category.Main outcome measures The presence and severity of cerebral WMLs.Results Formerly pre-eclamptic women had WMLs significantly more often (37%) and more severely (mean, 0.11; median, 0.00; range, 0-2.34 ml) than controls (21%, P = 0.04; mean, 0.015; median, 0.00; range, 0-0.13 ml; P = 0.02). Current hypertension and a history of early-onset pre-eclampsia (<37 weeks) were independently associated with the presence of WMLs (b = 1.34, P = 0.02 and b = 1.73, P = 0.01, respectively).Conclusions Our findings indicate that pre-eclampsia might be a risk marker for early cerebrovascular damage. The predisposition of formerly pre-eclamptic women to later cardiovascular and cerebrovascular disease may be an important factor for the development of cerebral WMLs. Whether a history of posterior reversible encephalopathy syndrome may be an additive risk factor for the development of these lesions remains unknown.

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Objective: To study whether lower arterial oxygen saturation (SaO 2 ) and chronic obstructive pulmonary disease (COPD) are associated with cerebral white matter lesions and lacunar infarcts. Methods: We measured SaO 2 twice with a pulse oximeter, assessed the presence of COPD, and performed MRI in 1077 non-demented people from a general population (aged 60-90 years). We rated periventricular white matter lesions (on a scale of 0-9) and approximated a total subcortical white matter lesion volume (range 0-29.5 ml). All analyses were adjusted for age and sex and additionally for hypertension, diabetes, body mass index, pack years smoked, cholesterol, haemoglobin, myocardial infarction, and left ventricular hypertrophy. Results: Lower SaO 2 was independent of potential confounders associated with more severe periventricular white matter lesions (score increased by 0.12 per 1% decrease in SaO 2 (95% confidence interval 0.01 to 0.23)). Participants with COPD had more severe periventricular white matter lesions than those without (adjusted mean difference in score 0.70 (95% confidence interval 0.23 to 1.16)). Lower SaO 2 and COPD were not associated with subcortical white matter lesions or lacunar infarcts. Conclusion: Lower SaO 2 and COPD are associated with more severe periventricular white matter lesions. C erebral white matter lesions and lacunar brain infarcts are frequently observed on magnetic resonance imaging scans of elderly people. [1][2][3][4] Evidence is accumulating that these lesions play an important role in the development of cognitive decline and dementia. [5][6][7] Although the exact pathogenesis of these lesion is not fully understood, they are considered to be caused by ischaemic small vessel disease, with hypertension and increased age as the most important risk factors. Degenerative changes of cerebral small vessels result in narrowing and obstruction of the arteriolar lumen and alteration of the cerebral autoregulation, both resulting in hypoperfusion of the cerebral white matter and basal ganglia. 8In addition to cerebral perfusion, the arterial oxygen content determines the total amount of oxygen available in the brain. Low arterial oxygen pressure strongly aggravates brain damage caused by cerebral hypoperfusion. Pure hypoxaemic insults, however, fail to cause brain damage. 9Whether lower arterial oxygen pressure in elderly people plays a role in the pathophysiology of white matter lesions is unknown.The assessment of the arterial oxygen pressure is a relatively invasive procedure and therefore not applicable in a large population based study. The oxygen saturation of haemoglobin, as assessed by pulse oximetry, is a non-invasive measurement that gives an indication of the arterial oxygen pressure. We studied the association between arterial oxygen saturation (SaO 2 ) and white matter lesions and lacunar infarcts. Chronic obstructive pulmonary disease (COPD) is a common disease among elderly people. [10][11][12][13] Patients with COPD experience oxygen deprivation for prolonged periods, especi...

Our findings indicate that the amount of T2 lesions has a small predictive value for progression of disability in relapsing remitting MS, but has no influence on the rate of progression in progressive MS.