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Hypertension+MRI changes=impaired cognition
  1. S Tuhrim,
  2. S R Levine
  1. The Stroke Program, Department of Neurology, The Mount Sinai School of Medicine, New York, USA
  1. Correspondence to:
 Dr S R Levine, Stroke Program, Department of Neurology, Box 1137, The Mount Sinai School of Medicine, One Gustave L Levy Place, New York 10029–6574, USA;

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A quantifiable formula?

As both the average age of the population and rates of vascular dementia increase, there has been keen interest in measuring and quantifying determinants of cognitive impairment. Koga et al (this issue pp 737–741)1 quantify brain MRI abnormalities and relate them to loss of a normal mental state in a single rural, independent, elderly community. Cognitive impairment was defined as a mini mental state examination (MMSE) score <24 with a mean study score of 26 points.1

The work exemplifies the expanding body of investigations utilising increasingly complex MRI techniques and data analyses to provide insights into brain function beyond those obtainable by mere visual inspection of images. Emerging new structural imaging techniques such as diffusion tensor imaging, can provide information regarding white matter characteristics associated with disease states and brain response to injury (neuroplasticity) and take us beyond more conventional MRI images. The work of Koga et al not only provides confirmation of the importance of white matter lesions and generalised atrophy as markers of cognitive decline but also provides a potentially useful tool for quantifying these changes.

It is important not to lose sight, amid this march of technical development, of their confirmation of an important epidemiological finding: the association of systolic blood pressure with decreased cognition. Although this factor did not appear in the multivariate logistic model, most likely because of its colinearity with the MRI measurements of white matter lucencies and decreased brain volume, factors with which it is known to be associated, its link to cognitive decline and decreased cerebral perfusion has long been appreciated.2 Recently, analysis of the national Health and Nutrition Examination Survey (NHANES) in the United States indicated that 27% of the United States population had hypertension but only 23% of these with hypertension were taking medication that controlled their blood pressure. Among those with untreated or uncontrolled hypertension, isolated increased systolic blood pressure was the most common pattern found.3 Indeed isolated mild systolic hypertension is the most prevalent form of uncontrolled hypertension in the United States. The work of Koga et al provides further evidence of the importance of addressing this silent epidemic.

We also know from the Cardiovascular Health Study (CHS)4 that focal lesions >3 mm on brain MRI (“silent strokes”) were present in 28% of 3324 participants in this study. The presence of these MRI lesions doubled the risk of subsequent stroke, as did increased diastolic and systolic blood pressure, internal carotid artery wall thickness, and the presence of atrial fibrillation. Silent strokes as seen on MRI were an independent predictor of symptomatic stroke, at a rate of 18.7/1000 person-years, over the 4 years of follow up in older people without a clinical history of stroke.

Based on the recent results of the PROGRESS trial,5 we should be considering more aggressive blood pressure management in patients with cerebrovascular disease, even in patients with borderline or normal blood pressures (in high risk patients) as data strongly suggest a causal link between blood pressure, MRI lesions, and silent and symptomatic cerebrovascular disease. We are making progress on solving the equation that has blood pressure, MRI changes, and cognition as the variables.

A quantifiable formula?