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Updated: Mar 8, 2026

Assessing Cortical Cerebral Microinfarcts on High Resolution MR Images

Assessing Cortical Cerebral Microinfarcts on High Resolution MR Images

Published on: November 20, 2015

Functional deficits induced by cortical microinfarcts.

Philipp M Summers¹, David A Hartmann¹, Edward S Hui²

¹1 Department of Neurosciences, Medical University of South Carolina, Charleston, SC, USA.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism

|January 17, 2017

Summary

This summary is machine-generated.

Tiny cerebral microinfarcts cause widespread brain dysfunction, impacting brain function far beyond visible damage. This study reveals how these small injuries contribute to cognitive impairment in vascular dementia.

Keywords:

Microinfarcts microcirculation neurovascular coupling two-photon microscopy vascular cognitive impairment

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Compensatory Limb Use and Behavioral Assessment of Motor Skill Learning Following Sensorimotor Cortex Injury in a Mouse Model of Ischemic Stroke

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Published on: July 10, 2014

Area of Science:

Neuroscience
Vascular Biology
Medical Imaging

Background:

Cerebral microinfarcts are linked to cognitive impairment.
The extent of functional disruption by microinfarcts is not fully understood.
Microinfarcts represent a small percentage of total brain volume.

Purpose of the Study:

To investigate if microinfarcts cause functional deficits beyond visible tissue damage.
To quantify the extent of functional disruption caused by microinfarcts.
To explore the persistence of these functional deficits.

Main Methods:

Utilized a mouse model with targeted photothrombosis to induce single microinfarcts.
Employed in vivo structural and diffusion MRI for acute microinfarct core detection.
Used c-Fos assays and in vivo hemodynamic imaging to assess neuronal activity and blood flow.
Validated MRI findings with post-mortem neuronal viability stains.

Main Results:

In vivo MRI accurately identified acute microinfarct cores.
Functional deficits, including impaired neuronal activity and hemodynamics, were observed in viable tissue surrounding microinfarcts.
The volume of functionally impaired tissue was estimated to be at least 12-fold larger than the microinfarct core.
Hemodynamic deficits persisted for at least 14 days, suggesting lasting neuronal circuitry or neurovascular coupling issues.

Conclusions:

Microinfarcts disrupt brain function in areas significantly larger than the visible lesion.
These widespread functional deficits contribute to cognitive impairment seen in vascular dementia.
Understanding the broader impact of microinfarcts is crucial for developing effective treatments for cognitive decline.