eMedicine Specialties > Neurology > Neuro-imaging

Magnetic Resonance Imaging in Acute Stroke

Author: Souvik Sen, MD, MS, FAHA,, Associate Professor of Neurology, Founding Director of UNC Hospital Stroke Center, Director of Neurovascular Residency, Department of Neurology, University of North Carolina at Chapel Hill
Contributor Information and Disclosures

Updated: Jul 15, 2009

Introduction

Background

MRI is a new and promising tool that is being increasingly used in the diagnosis and management of acute ischemic stroke. The aim of this article is to provide simple and up-to-date information about the use of MRI in acute ischemic stroke. MRI is a fast-growing technology that is sensitive and relatively specific in detecting changes that occur after such strokes. It has some limitations, such as high cost, long scanning duration, and decreased sensitivity in the detection of subarachnoid hemorrhages; these constitute exciting challenges in the future of this technology. Recent advances in MRI, including higher strength of magnetic field (1.5-3.0 T field strength) yielding better resolution of images, newer sequences of images, and the advent of the open MRI for patients who are claustrophobic or overweight, have lead to widespread use of this technology in diagnosis and management of acute stroke.

Pathophysiology

Some nuclei in the human body become excited when positioned in a strong magnetic field; they absorb the radiofrequency energy of the magnetic field and then release it until they relax completely. The energy is released from the excited tissue over a short period of time according to 2 relaxation constants known as T1 and T2, and the emitted energy signals are converted into images. The contrasts in the images result from different intensities of these emitted signals, which in turn result from different concentrations of the nuclei in different tissues in the body.

Hydrogen (ie, protons) is the most common magnetic resonance (MR)–observable nucleus in the human body and has the advantage of being present in many different tissues in different concentrations. Other organic particles have been tried but demonstrated less spatial resolution than hydrogen. Other biochemical compounds, lactate and N-acetyl aspartate, are under trial to increase understanding of the significance of the different concentrations of these compounds in different pathologic conditions (ie, MR spectroscopy).

Commonly used MR imaging techniques are the following:

  • T1-weighted imaging (T1-WI) in which cerebrospinal fluid (CSF) has a low signal intensity in relation to brain tissue
  • T2-weighted imaging (T2-WI) in which CSF has a high signal intensity in relation to brain tissue
  • Spin density–weighted imaging in which CSF has a density similar to brain tissue
  • Gradient echo imaging, which has the highest sensitivity in detecting early hemorrhagic changes
  • Diffusion-weighted imaging (DWI) in which the images reflect microscopic random motion of water molecules
  • Perfusion-weighted imaging (PWI) in which hemodynamically weighted MR sequences are based on passage of MR contrast through brain tissue

Pathogenesis of imaging findings

Regardless of the cause, neuronal ischemia rapidly depletes intracellular adenosine triphosphate (ATP), which leads to failure of the membrane-bound ATP-dependent ionic channels responsible for both neuron resting membrane potentials as well as generation of action potentials. This metabolic aberration results in accumulation of intracellular ions (including calcium ions), creating an intracellular gradient responsible for intracellular accumulation of water (ie, cytotoxic edema).

Cerebral endothelial cells are more resistant to ischemia than are neurons and neuroglial cells. About 3-4 hours after the onset of ischemia, the integrity of the blood-brain barrier becomes compromised, and plasma proteins are able to pass into the extracellular space. The intravascular water follows when reperfusion occurs (vasogenic edema); this process begins 6 hours after the onset of stroke and reaches a maximum 2-4 days after the onset of stroke. Reperfusion can also be accompanied by hemorrhagic transformation of the infarct, which is usually related to the volume and site of the infarct, being more common in large cortical infarcts.

Changes in MR images due to ischemic stroke follow the vascular territory of the occluded blood vessel, which is characteristic of cerebrovascular disease and helps in differentiating it from other disease entities.

More on Magnetic Resonance Imaging in Acute Stroke

Overview: Magnetic Resonance Imaging in Acute Stroke
Differential Diagnoses & Workup: Magnetic Resonance Imaging in Acute Stroke
Follow-up: Magnetic Resonance Imaging in Acute Stroke
Multimedia: Magnetic Resonance Imaging in Acute Stroke
References
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Further Reading

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Keywords

cerebrovascular accident, CVA, acute ischemic stroke, cerebrovascular disease, T1-weighted imaging, T2-weighted imaging, spin density–weighted imaging, gradient echo imaging, diffusion-weighted imaging, perfusion-weighted imaging, MRI, MRI in acute stroke

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Contributor Information and Disclosures

Author

Souvik Sen, MD, MS, FAHA,, Associate Professor of Neurology, Founding Director of UNC Hospital Stroke Center, Director of Neurovascular Residency, Department of Neurology, University of North Carolina at Chapel Hill
Souvik Sen, MD, MS, FAHA, is a member of the following medical societies: American Academy of Neurology, American Heart Association, and Association for Patient Oriented Research
Disclosure: Nothing to disclose.

Medical Editor

Draga Jichici, MD, FRCP, Associate Clinical Professor, Department of Medicine, Division of Neurology and Critical Care Medicine, McMaster University, Canada
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center
Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association
Disclosure: Boehringer Ingelheim Honoraria Speaking and teaching; BMS/Sanofi Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health & Science University; Associate Director, Oregon Stroke Center
Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association
Disclosure: Co-Axia Consulting fee Review panel membership; Talecris Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Boehringer Ingelheim Honoraria Speaking and teaching; Concentric Medical Consulting fee Review panel membership; Abbott Consulting fee Consulting; Sanofi  Consulting

 
 
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