Early microvascular dysfunction in cerebral small vessel disease is not detectable on 3.0 Tesla magnetic resonance imaging: a longitudinal study in spontaneously hypertensive stroke-prone rats

Experimental & Translational Stroke Medicine

Stefanie Schreiber⁵  Christoph Kleinschnitz¹  Klaus G Reymann⁵  Hans-Jochen Heinze⁵  György Homola³  Eva Göb¹  Holger Braun⁵  Solveig Niklass²  Cornelia Garz⁴  Stine Mencl¹ 

[1] Department of Neurology, University Hospital of Würzburg, Würzburg, Germany;Leibniz Institute for Neurobiology, Magdeburg, Germany;Department of Neuroradiology, University Hospital of Würzburg, Würzburg, Germany;Department of Neurology, Otto-von-Guericke-University, Magdeburg, Germany;German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany

关键词: MRI;    SHRSP;    Cerebral small vessel disease;   

Others  :  861566
DOI  :  10.1186/2040-7378-5-8

 received in 2013-06-21, accepted in 2013-06-21,  发布年份 2013

【 摘 要 】

Background

Human cerebral small vessel disease (CSVD) has distinct histopathologic and imaging findings in its advanced stages. In spontaneously hypertensive stroke-prone rats (SHRSP), a well-established animal model of CSVD, we recently demonstrated that cerebral microangiopathy is initiated by early microvascular dysfunction leading to the breakdown of the blood–brain barrier and an activated coagulatory state resulting in capillary and arteriolar erythrocyte accumulations (stases). In the present study, we investigated whether initial microvascular dysfunction and other stages of the pathologic CSVD cascade can be detected by serial magnetic resonance imaging (MRI).

Findings

Fourteen SHRSP and three control (Wistar) rats (aged 26–44 weeks) were investigated biweekly by 3.0 Tesla (3 T) MRI. After perfusion, brains were stained with hematoxylin–eosin and histology was correlated with MRI data. Three SHRSP developed terminal CSVD stages including cortical, hippocampal, and striatal infarcts and macrohemorrhages, which could be detected consistently by MRI. Corresponding histology showed small vessel thromboses and increased numbers of small perivascular bleeds in the infarcted areas. However, 3 T MRI failed to visualize intravascular erythrocyte accumulations, even in those brain regions with the highest densities of affected vessels and the largest vessels affected by stases, as well as failing to detect small perivascular bleeds.

Conclusion

Serial MRI at a field strength of 3 T failed to detect the initial microvascular dysfunction and subsequent small perivascular bleeds in SHRSP; only terminal stages of cerebral microangiopathy were reliably detected. Further investigations at higher magnetic field strengths (7 T) using blood- and flow-sensitive sequences are currently underway.

【 授权许可】

   
2013 Mencl et al.; licensee BioMed Central Ltd.

【 图 表 】

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