Changes in the MRI brain picture associated with newly diagnosed asymptomatic arterial hypertension

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ntroduction. Arterial hypertension (AH) is the major modified risk factor for brain injury. Clarification of the brain changes and the mechanisms of their development during the asymptomatic stage will ensure better results in the prevention of AH complications.
Objective. The study purpose was to evaluate specific changes in the brain MRI picture, associated with AH of varying severity.
Materials and methods. The study involved 82 patients with newly diagnosed asymptomatic AH, aged 45–59 years. The patients underwent MRI of the brain (T1 and T2 weighted images, FLAIR, diffusion weighted imaging with calculation of an apparent diffusion coefficient (ADC) map). We evaluated the localization and severity of white matter hyperintensity (WMH), lacunar infarcts, and dilated perivascular spaces as well as the white matter microstructure based on ADC in a visually intact white matter in areas of its potential vulnerability.
Results. The earliest and most typical change is the formation of hyperintensity lesions in the juxtacortical areas of the frontal lobes. AH worsening is associated with an increase in the number of hyperintensity lesions from the frontal to occipital areas of the white brain matter and from the surface to deep brain regions as well as microstructural changes in the intact white matter in potential vulnerability areas.
Conclusion. The observed high correlations between WMH and dilated semioval perivascular spaces and increased diffusion in the intact white matter as well as the absence of similar correlations for lacunar infarcts suggest that the pathophysiological basis of early brain changes in AH is increased vascular permeability, but not ischemia. The factors of a high risk of clinical symptoms include lesion extension to the posterior brain structures, multiple foci of hyperintensity in the periventricular white matter of the frontal lobes, and an increasing number of lacunar infarcts. These findings are significant for evaluating potential risk of clinical symptoms and for understanding the mechanisms of early brain injury in AH.

About the authors

Larisa A. Dobrynina

Research Center of Neurology

Author for correspondence.
ORCID iD: 0000-0001-9929-2725

D. Sci. (Med.), Head, 3rd Neurology department

Russian Federation, Moscow

Elena V. Gnedovskaya

Research Center of Neurology

Russian Federation, Moscow

Anastasiya N. Sergeeva

Research Center of Neurology

Russian Federation, Moscow

Marina V. Krotenkova

Research Center of Neurology

ORCID iD: 0000-0003-3820-4554

D. Sci. (Med.), Head, Neuroradiology department

Russian Federation, 125367 Moscow, Volokolamskoye shosse, 80

Мikhail A. Piradov

Research Center of Neurology

ORCID iD: 0000-0002-6338-0392

D. Sci. (Med), Prof., Full Member of RAS, Director, Research Center of Neurology, Moscow, Russia; Head, Division of diseases of the nervous system

Russian Federation, 125367 Moscow, Volokolamskoye shosse, 80


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Copyright (c) 2016 Dobrynina L.A., Gnedovskaya E.V., Sergeeva A.N., Krotenkova M.V., Piradov M.A.

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