AUTHOR AND EDITOR INFORMATION

Section 1 of 8  

• Authors and Editors
• Introduction
• Differentials
• Workup
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 8  

• Authors and Editors
• Introduction
• Differentials
• Workup
• Follow-up
• Miscellaneous
• Multimedia
• References

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.

DIFFERENTIALS

Section 3 of 8  

• Authors and Editors
• Introduction
• Differentials
• Workup
• Follow-up
• Miscellaneous
• Multimedia
• References

WORKUP

Section 4 of 8  

• Authors and Editors
• Introduction
• Differentials
• Workup
• Follow-up
• Miscellaneous
• Multimedia
• References

Imaging Studies

• Radiography - A regular radiograph may be indicated if any possibility exists of a metallic implant or foreign body, pacemaker, aneurysm clip, or recently implanted prosthetic heart valve.
• MRI techniques - Diffusion-weighted imaging
• • DWI is sensitive to the microscopic random motion of the water molecule protons, a value known as the apparent diffusion coefficient (ADC), which is measured and captured by this type of imaging. The water molecules move in the direction of the magnetic field gradient; they accumulate a phase shift in their transverse magnetization relative to that of a stationary one, and this phase shift is directly related to the signal attenuation of the image.
  • Numerous studies have shown that ADCs in ischemic areas are lower by 50% or more than those of normal brain areas, and they appear as bright areas (ie, hyperintensities) on the DWI (see Image 1). Studies have demonstrated that changes in the ADC occur as early as 10 minutes following onset of ischemia.
  • Cytotoxic edema appears following sodium/potassium pump failure, which results from energy metabolism failure due to ischemic insult; this occurs within minutes of the onset of ischemia and produces an increase in brain tissue water of up to 3-5%. Reduction in intracellular and extracellular water molecule movement is the presumed explanation for the drop in ADC values.
  • The diffusion of water molecules is guarded by biologic barriers in the brain tissue (eg, cell membranes and cellular organelles). The behavior of water molecules is not symmetric and may show uneven distribution of the ADC when measured in one direction; this uneven distribution may give a false impression of a lesion. ADC values are measured in several directions (3, 6, or more), and ADC maps are created to produce a direction-insensitive measurement of the diffusion. When ADC is measured in 6 or more directions, the diffusion motion of all the water molecules (ie, ADC tensor matrix) can be calculated to create what is called full diffusion tensor mapping, which can also be used to visualize white matter tracts.
  • Reduction in the ADC also occurs in other conditions such as global ischemia, hypoglycemia, and status epilepticus; it should always be evaluated in relation to the clinical condition of the patient.
  • Human studies demonstrated that damage in the areas showing decreased ADC levels is very rarely reversible (in contrast to that in animal models), although a few studies have indicated that intra-arterial thrombolysis may occasionally result in disappearance of the diffusion defect. The technique most commonly used to acquire the DWI is an ultrafast one, echo-planar imaging (EPI); this technique decreases scanning time significantly and eliminates movement artifacts.
  • The acute drop in ADC is gradually normalized to baseline at 5-10 days after ischemia (pseudonormalization); it even exceeds normal levels as time passes, helping in some cases to differentiate between acute, subacute, and chronic lesions.
  • DWI is very sensitive and relatively specific in detecting acute ischemic stroke. DWI findings have shown high levels of diagnostic accuracy; however, recent studies demonstrated that small brainstem lacunar infarctions may escape detection. Normal DWI in patients with strokelike symptoms should trigger further investigation for a nonischemic cause of the symptoms. DWI has been shown to reveal diffusion abnormalities in almost 50% of patients with clinically defined transient ischemic attacks (TIAs); it tends to be of higher yield at increasing time intervals from the onset of stroke symptoms.
  • From the clinical experience at the Stroke Center at JFK Medical Center of Seton Hall University, the following differential for areas of hyperintensity on DWI was generated:
  • • Subacute ischemic stroke - Usually takes 7-14 days for hyperintensity to subside
    • Hemorrhagic stroke - Usually bright on T1-WI
    • Multiple sclerosis plaque - Also bright on FLAIR and T2-WI
    • Traumatic brain injury - History of trauma
    • Brain abscess - Ring enhancement on contrast MRI
    • Choroid plexus - Usually intraventricular in location, may be bilateral
    • Epidermoid - Usually extra-axial in location
    • Air-bone interface - Commonly bilateral, in the temporal bone
• MRI techniques - Perfusion-weighted imaging
• • With this technique, information about the perfusion status of the brain is available. The most commonly used technique is bolus-contrast tracking (other techniques include blood oxygen level and arterial spin tagging). The imaging is based on the monitoring of a nondiffusible contrast material (gadolinium) passing through brain tissue.
  • The signal intensity declines as contrast material passes through the infarcted area and returns to normal as it exits this area. A curve is derived from this tracing data (ie, signal washout curve), which represents and estimates the cerebral blood volume (CBV).
  • An arterial input function can be derived by measuring an artery in lower brain slices or by measuring gadolinium concentration that is proportional to the changes in T2 when gadolinium is used at low doses (<3 mg/kg). Based on this arterial input function, quantitative maps of cerebral blood flow (CBF), CBV, mean transit time (MTT), time to peak (TTP), and various other hemodynamic parameters can be obtained. Considerable debate surrounds the choice of which PWI parameter should be used. Most centers in the United States use time domain parameters such as MTT or TTP.
  • DWI and PWI together have been shown to be superior to conventional MRI both in early phases and also up to 48 hours after the onset of stroke. Using both DWI and PWI is very important because together they provide information about location and extent of infarction within minutes of onset; when performed in series, they can provide information about the pattern of evolution of the ischemic lesion. This information may be of great importance in choosing the appropriate treatment modality as well as in predicting outcome and prognosis. Several recent randomized clinical trials are selecting patients with diffusion-perfusion mismatch to test thrombolytic treatment alternatives beyond the standard 3-hour time window used for IV TPA. These studies have been reviewed by Davis et al (Davis, 2005).
  • The lesion usually enlarges on serial DWIs over a period of several days. It has been suggested that this enlargement can be halted if reperfusion (ie, resolution of original PWI lesion) occurs early enough. Lesions that are not large on initial PWI do not show this enlargement.
  • The diffusion-perfusion mismatch (see Image 3), ie, the difference in size between lesions captured by DWI and PWI, usually represents the ischemic penumbra (see Image 3), which is the region of incomplete ischemia that lies next to the core of the infarction. The ischemic penumbra is regarded as an area that is viable but under ischemic threat; it can be saved if appropriate intervention is promptly instituted. The viability of this region could extend up to 48 hours after the onset of stroke. Determining the volume of the ischemic penumbra may be very useful in identifying patients who would benefit from thrombolytic therapy and perhaps even conventional treatments such as carotid endarterectomy or blood pressure elevation. It could also aid in evaluating the risk/benefit ratio of using such treatments in stroke patients.
  • One limitation of these techniques is in detection of acute intracerebral hemorrhages; early studies demonstrated that susceptibility imaging could be sensitive in the detection of acute intracerebral hemorrhage. Gradient-recalled echo (GRE) imaging sequences demonstrated the most favorable sensitivity in detecting susceptibility dephasing associated with chronic intracerebral hemorrhages.
  • MRI still has some limitations in its application, namely, in patients with metal implants and acutely ill patients requiring close monitoring.
  • These new techniques, DWI and PWI, together represent the most exciting areas in MRI for their potential ability to detect early changes (ie, within minutes of the stroke). They are currently used in the evaluation of thrombolytic and neuroprotective therapy in acute stroke clinical trials.
• MRI techniques – Blood oxygen level-dependent (BOLD) MRI
• • Oxygen extraction fraction (OEF) measured by positron emission tomography (PET) imaging is considered the criterion standard for imaging the ischemic penumbra in acute ischemic stroke. Until now, MR diffusion-perfusion imaging has been the only MR technique that measures this reversibly damaged brain area.
  • BOLD is a new technique that can be used to detect deoxyhemoglobin in the cerebral capillaries and veins as an MRI indicator of brain OEF. Recent evidence suggests that BOLD MRI might provide a better estimation of the ischemic penumbra in acute ischemic stroke compared with MR diffusion-perfusion mismatch.
  • Further validation of the technique is required to confirm its clinical value in imaging of acute ischemic stroke.
• MRI techniques - Echo-planar imaging
• • EPI is a recent technique that can be used to visualize physiologic parameters in addition to measuring diffusion coefficients of the ischemic brain. Changes in brain oxygenation can be monitored by using gradient echo and EPI, in which deoxygenated blood acts as a susceptibility contrast agent.
  • EPI can be used in conjunction with bolus injection of intravenous paramagnetic agents to assess cerebral perfusion and functional changes in CBV.
  • In this technique, hypoperfused areas appear as hyperintense signals after injection of the contrast material. This technique is considered a way of reducing the traditionally long scanning time of MRI.
• MRI techniques - Magnetic resonance spectroscopy
• • Magnetic resonance spectroscopy (MRS) is one of the recent advances in MR technology; it evaluates metabolic activity and concentration of certain metabolites in specified areas of the brain. Proton and phosphorus spectroscopic studies have been performed.
  • In proton spectroscopy, depression of N-acetyl aspartate, which is considered to be a marker of neurons, is the most consistent finding in acute stroke. This depression may occur within hours after the onset of stroke and continues through the subacute and chronic phases of the stroke, presumably because of loss of neurons.
  • Increase in levels of lactate is another important finding and has been attributed to anaerobic metabolism in ischemic tissue. Initial studies of other metabolites, such as choline and creatine, demonstrated decreases in their levels in acute stroke.
  • Phosphorus spectroscopy provides information about energy metabolism and pH, depletion of ATP, decrease of tissue pH, and increase of the ratio of inorganic phosphate to phosphocreatine, which has been reported in both human and animal studies.
  • Long acquisition times, weak signal, and low spatial resolution of this technique have limited enthusiasm for its use in the clinical management of cerebral ischemia; however, some studies have suggested that MRS results can have prognostic value in stroke.
• MRI techniques - Magnetic resonance angiography
• • Magnetic resonance angiography (MRA) is very sensitive to flow and is based on the difference in signal between moving blood and stationary brain tissue; angiographiclike images of the cervicocranial vasculature are produced.
  • MRA images are a useful tool in identifying dissections, in that both the true and false lumen of the involved artery can be observed on the source images. Following is a brief description of the 2 basic techniques.
  • The three-dimensional (3D) time-of-flight (TOF) technique is based on flow-related enhancement; it is the preferred MRA technique. However, it has some limitations, especially flow signal dropout secondary to turbulent flow in the tortuous and stenotic vascular segments, which makes interpretation of stenosis in these areas difficult. These are common predilection sites for atherosclerosis. Also, in slow-flow regions, the spin saturation of the scan causes overestimation of stenosis. In contrast-enhanced studies, it provides more information than standard angiography, especially in detecting critical stenosis of extracranial vessels, but it is less reliable in intracranial critical stenosis. Always keep in mind that MRA is a flow-dependent technology; absence of flow signal does not mean literally a complete occlusion but rather that flow is below a critical value.
  • Two-dimensional (2D) TOF MRA also depends on the relative contrast between flowing blood and stationary tissue; it provides better images than 3D TOF in slow-flow regions. 2D TOF images correlate well with carotid angiography images in depicting cervical bifurcation disease. Its disadvantages, however, are the significant artifacts (eg, stepladder) that often occur, which may obscure vessel details, and the longer scanning time.
  • The modified TOF MRA technique, which uses multiple overlapping thin slab acquisitions (MOTSA), combines the advantages of 2D and 3D TOF techniques. It is very helpful in demonstrating severe stenosis, although the degree of stenosis might be slightly overestimated.
  • Two-dimensional phase-contrast (PC) MRA is a technique that is helpful specifically in differentiating slow and absent flow from normal flow; it captures only truly patent vessels. Other imaging sequences (eg, spin-echo sequence or gradient-echo sequence) should be used with PC-MRA to avoid missing lesions such as paravascular hematomas, which are not captured by PC-MRA. PC-MRA also has the disadvantage of signal loss due to turbulent flow in tortuous vessels.
• Types of infarction
• • Thromboembolic infarction: This is the most common form of infarction. Typically, it is observed on MRI as a wedge-shaped infarct in the particular vascular distribution. Recent data support the hypothesis that a single infarct in a vascular territory is more likely to be thrombotic than multiple infarcts, which are more likely to be embolic.
  • Watershed infarction: This type of infarction occurs at the distal margins of specific arterial territories. It can occur both superficially and deep in the brain parenchyma. Common etiologies for this lesion include hypotension, cardiac and respiratory arrest, and proximal arterial stenosis or occlusion. MRI findings follow the pattern of incomplete thromboembolic ischemic infarction in T1 and T2 morphologic and signal changes, with early parenchymal enhancement suggesting early reperfusion. Recent studies show that this type of infarction could be more readily detected by using DWI.
  • Lacunar infarction: These are small deep cerebral infarctions believed to be caused by intrinsic small-vessel disease secondary to lipohyalinosis and fibrinoid necrosis; they are most frequently observed in patients with hypertension or diabetes mellitus. Common sites for these lesions include basal ganglia, internal capsule, thalamus, brain stem, and cerebellum. MRI findings in these lesions follow the same pattern observed in thromboembolic infarction.
  • Venous thrombosis and infarction: Occlusion of cerebral veins and venous sinuses is usually caused by systemic conditions, such as pregnancy, collagen vascular diseases, inflammatory bowel diseases, and hypercoagulable states, as well as local conditions such as infection, neoplasia, and trauma. Occlusion of the venous structure causes outflow obstruction and vascular congestion that results in parenchymal infarctions and hemorrhages.
  • • Patients usually present in the late acute phase or in the subacute phase, which makes the diagnosis difficult because diagnosis at these stages depends on imaging studies.
    • MRI findings in these lesions include loss of venous flow void signal, absence of normal venous enhancement, and visualization of isointense to hyperintense signals within the venous channels on both T1 and T2 images. These variable patterns of enhancement are due to mixed blood products, which are present in the lesion.
    • These patterns are usually bilateral, do not respect arterial vascular territories, and have associated hemorrhage.
    • Three-dimensional phase contrast magnetic resonance venography (MRV) is the preferred technique in the evaluation of venous thrombosis.
• MRI findings in acute stroke - Hyperacute phase (0-24 h)
  • DWI is able to detect ischemic changes within minutes of onset (see Image 1). Reduced proton motion is detected as a decreased ADC.
  • Early in the process of cerebral ischemia, PWI, using first-pass contrast bolus injection or spin tagging the protons in the water in blood, reveals reductions of CBF and CBV and an increased MTT of blood through the brain (see Image 2).
  • Matched diffusion- and perfusion-weighted abnormalities correlate with the region of infarction and are indicative of permanent neuronal death. Mismatched diffusion and perfusion abnormalities with the perfusion abnormality larger than the diffusion abnormality may be indicative of a region of reversible ischemic penumbra (see Image 3).
  • A few hours after stroke onset, a loss of arterial void signal is sometimes observed (30-40% of patients); it is best observed on T2-WI.
  • At 2-4 hours, T1-WI shows subtle effacement of the sulci due to cytotoxic edema.
  • At 8 hours, T2-WI shows hyperintense signal due to both cytotoxic and vasogenic edema.
  • At 16-24 hours, T1-WI shows hypointense signal due to both cytotoxic and vasogenic edema.
  • Contrast-enhanced images show arterial enhancement followed by parenchymal enhancement. The arterial enhancement can be very early (in more than 50% of patients) and is due to slow blood flow; it typically disappears after 1 week.
  • Parenchymal enhancement differs in complete and incomplete infarctions. In complete infarction, it starts 5-7 days after the stroke and persists for several months. In incomplete infarctions, it can be observed within 2-4 hours and usually is more intense than in complete infarction.
  • Although conventional MRI sequences most often do not show evidence of stroke in the acute phase, conventional MRI may show signs of intravascular thrombus such as absence of flow void on T2-WI, vascular hyperintensity on FLAIR, and hypointense vascular sign on GRE sequence.
  MRI findings in acute ischemic changes

  Time	MRI Finding	Etiology
  2-3 min	DWI - Reduced ADC	Decreased motion of protons
  2-3 min	PWI - Reduced CBF, CBV, MTT	Decreased CBF
  0-2 h	T2-WI - Absent flow void signal	Slow flow or occlusion
  0-2 h	T1-WI - Arterial enhancement	Slow flow
  2-4 h	T1-WI - Subtle sulcal effacement	Cytotoxic edema
  2-4 h	T1-WI - Parenchymal enhancement	Incomplete infarction
  8 h	T2-WI - Hyperintense signal	Vasogenic and cytotoxic edema
  16-24 h	T1-WI - Hypointense signal	Vasogenic and cytotoxic edema
  5-7 d	Parenchymal enhancement	Complete infarction

• MRI findings in acute stroke - Acute phase (1-7 d)
• • In this phase, edema increases (edema maximizes at 48-72 h), and MRI signals become more prominent and well demarcated. The ischemic area continues to appear as an area of hypointensity on T1-WI and as a hyperintense area on T2-WI. Also, the mass effect can be appreciated in this phase.
  • In contrast-enhanced images, the arterial enhancement usually persists throughout the acute phase, while the parenchymal enhancement is usually appreciated at the end of this phase in complete infarction. In incomplete infarction, the parenchymal enhancement is usually earlier.
  • During this period, reperfusion occurs and both petechial and frank hemorrhage can be observed, typically 24-48 hours after the onset of the stroke. Usually, petechial hemorrhages cause the "fogging" phenomenon, due to hemoglobin degradation products, that masks the infarction on both T1-WI and T2-WI.
• MRI findings in acute stroke - Subacute phase (7-21 d)
• • In this phase, the edema resolves and the mass effect becomes less appreciated; however, the infarcted areas still appear as a hypointensity on T1-WI and as a hyperintensity on T2-WI.
  • In contrast-enhanced images, the arterial enhancement is usually resolved by this time, and the parenchymal enhancement typically persists throughout this phase. The cortical parenchymal enhancement is usually in a gyriform pattern, while the subcortical enhancement is usually a homogenous central pattern.
• MRI findings in acute stroke - Chronic phase (>21 d)
• • In this phase, the edema completely resolves, and the infarcted area still appears as a hypointensity on T1-WI and as a hyperintensity on T2-WI. Because of tissue loss in the infarcted area by this time, ex-vacuo ventricular enlargement and widening of the cortical gyri and fissures take place.
  • In contrast-enhanced images, parenchymal enhancement typically persists throughout this phase also; it usually disappears by 3-4 months.
• MRI findings in TIA
• • A third to a half of the patients presenting with a TIA have lesions on DWI. A significant proportion of these patients may not reveal a corresponding lesion on T2-WI. PWI may be more sensitive but has not been adequately tested in patients with TIA. DWI-positive TIA lesions do necessarily show as infarction on follow-up MRI.
  • Although TIAs have been traditionally defined as transient (<24h) neurologic deficit of vascular origin, the advent of MRI has lead to reconsideration of the definition. Whether DWI-positive TIAs are to be regarded as stroke or TIA is unclear.
• MRI in hemorrhagic stroke
• • GRE and EPI sequences have the ability to detect microbleeds that are clinically silent and not visualized by CT scanning or routine MR sequences. These microbleeds are visualized in a fifth to a quarter of patients with ischemic stroke and 5% of elderly asymptomatic individuals. The microbleeds depict hemosiderin deposit and have been histopathologically correlated with prior extravasations of blood. These microbleeds may represent bleeding-prone angiopathy and a higher rate of hemorrhagic transformation from anticoagulation, antithrombotic, and thrombolytic therapy.
  • GRE, EPI, and DWI (B0) are sensitive to detecting intraparenchymal hemorrhage (primary intracerebral hemorrhage and hemorrhagic transformation) in the hyperacute stages (first few hours), whereas the conventional T1-WI and T2-WI are sensitive in detecting subacute and chronic bleeding. FLAIR sequences may have a role in detecting extra-axial collections of blood (subdural hemorrhages). Having stated the above, the current guidelines do not advocate the use of MR in place of CT scanning to screen patients for thrombolysis.

FOLLOW-UP

Section 5 of 8  

• Authors and Editors
• Introduction
• Differentials
• Workup
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Inpatients may often continue to be monitored and receive treatment while undergoing MRI because MRI-compatible ECG monitors, intravenous infusion pumps, and ventilators are available.

In/Out Patient Meds

• A mild sedative may be ordered for patients with a history of claustrophobia. As an alternative, an open MRI may be ordered at the cost of lesser quality MR images.

Complications

• Patients with metallic implants may have a variety of potential complications, such as heating and pacemaker malfunction and its consequences. For patients with a metallic implant, checking with the manufacturer regarding its MR compatibility is advisable if such information is not available elsewhere.
• Claustrophobic patients may be unable to complete the sequence of MRI. In selected patients, mild sedation or imaging in an open MR system may be attempted. However, most open MR scanners provide lesser quality images.
• Rarely, patients may be allergic to the contrast agent (eg, gadolinium) used in MRI.

Patient Education

• For excellent patient education resources, visit eMedicine's Imaging Center and Stroke Center. Also, see eMedicine's patient education articles Magnetic Resonance Imaging (MRI) and Stroke.

MISCELLANEOUS

Section 6 of 8  

• Authors and Editors
• Introduction
• Differentials
• Workup
• Follow-up
• Miscellaneous
• Multimedia
• References

• Patients who have received recent thrombolysis or are critically ill from stroke are probably not well suited for MRI because they cannot be monitored by clinical examinations during the period of imaging. If MRI is essential, it should be performed with the bare minimum of sequences required to make the diagnosis, such as T1, T2, DWI or PWI, and MRA. Many institutions have established acute stroke protocols to minimize scanning time.
• Patients with acute stroke who are considered for MRI should be evaluated for contraindications to MRI such as claustrophobia, metallic implants, pacemakers, and MR-incompatible prosthetic heart valves.

MULTIMEDIA

Section 7 of 8  

• Authors and Editors
• Introduction
• Differentials
• Workup
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Magnetic resonance imaging in acute stroke. Left: Diffusion-weighted MRI in acute ischemic stroke performed 35 minutes after symptom onset. Right: Apparent diffusion coefficient (ADC) map obtained from the same patient at the same time.
	View Full Size Image
Media type:  MRI

Media file 2:  Magnetic resonance imaging in acute stroke. Left: Perfusion-weighted MRI of a patient who presented 1 hour after onset of stroke symptoms. Right: Mean transfer time (MTT) map of the same patient.
	View Full Size Image
Media type:  MRI

Media file 3:  Magnetic resonance imaging in acute stroke. Diffusion-perfusion mismatch in acute ischemic stroke. The perfusion abnormality (right) is larger than the diffusion abnormality (left), indicating the ischemic penumbra, which is at risk of infarction.
	View Full Size Image
Media type:  MRI

Media file 4:  The diffusion-weighted MRI reveals a region of hypointensity in the distribution of the right middle cerebral artery. Flanking the anterior and posterior regions of this abnormality are regions of hyperintensities, which represent regions of new infarct. The contiguity of these regions suggests that they are extensions of the old infarct.
	View Full Size Image
Media type:  MRI

REFERENCES

Section 8 of 8

• Authors and Editors
• Introduction
• Differentials
• Workup
• Follow-up
• Miscellaneous
• Multimedia
• References

• Baird AE, Warach S. Magnetic resonance imaging of acute stroke. J Cereb Blood Flow Metab. Jun 1998;18(6):583-609. [Medline].
• Blatter DD, Parker DL, Ahn SS, et al. Cerebral MR angiography with multiple overlapping thin slab acquisition. Part II. Early clinical experience. Radiology. May 1992;183(2):379-89. [Medline].
• Chalela JA, Haymore JB, Ezzeddine MA, et al. The hypointense MCA sign. Neurology. May 28 2002;58(10):1470. [Medline].
• Davis SM, Donnan GA, Butcher KS, Parsons M. Selection of thrombolytic therapy beyond 3 h using magnetic resonance imaging. Curr Opin Neurol. Feb 2005;18(1):47-52. [Medline].
• Duong TQ, Fisher M. Applications of diffusion/perfusion magnetic resonance imaging in experimental and clinical aspects of stroke. Curr Atheroscler Rep. Jul 2004;6(4):267-73. [Medline].
• Fisher M, Albers GW. Applications of diffusion-perfusion magnetic resonance imaging in acute ischemic stroke. Neurology. Jun 10 1999;52(9):1750-6. [Medline].
• Geisler BS, Brandhoff F, Fiehler J, et al. Blood-oxygen-level-dependent MRI allows metabolic description of tissue at risk in acute stroke patients. Stroke. Jul 2006;37(7):1778-84. [Medline].
• Kidwell CS, Alger JR, Di Salle F, et al. Diffusion MRI in patients with transient ischemic attacks. Stroke. Jun 1999;30(6):1174-80. [Medline].
• Kidwell CS, Saver JL, Villablanca JP, et al. Magnetic resonance imaging detection of microbleeds before thrombolysis: an emerging application. Stroke. Jan 2002;33(1):95-8. [Medline].
• Medlock MD, Olivero WC, Hanigan WC, et al. Children with cerebral venous thrombosis diagnosed with magnetic resonance imaging and magnetic resonance angiography. Neurosurgery. Nov 1992;31(5):870-6; discussion 876. [Medline].
• Mok V, Chang C, Wong A, et al. Neuroimaging determinants of cognitive performances in stroke associated with small vessel disease. J Neuroimaging. Apr 2005;15(2):129-37. [Medline].
• Moseley ME, Cohen Y, Mintorovitch J, et al. Early detection of regional cerebral ischemia in cats: comparison of diffusion- and T2-weighted MRI and spectroscopy. Magn Reson Med. May 1990;14(2):330-46. [Medline].
• Moseley ME, Kucharczyk J, Mintorovitch J, et al. Diffusion-weighted MR imaging of acute stroke: correlation with T2-weighted and magnetic susceptibility-enhanced MR imaging in cats. AJNR Am J Neuroradiol. May 1990;11(3):423-9. [Medline].
• Rincon F. Anticoagulation and thrombolysis for acute ischemic stroke and the role of diagnostic magnetic resonance imaging. Arch Neurol. May 2004;61(5):801-2; author reply 802. [Medline].
• Runge VM, Kirsch JE, Wells JW, Woolfolk CE. Assessment of cerebral perfusion by first-pass, dynamic, contrast-enhanced, steady-state free-precession MR imaging: an animal study. AJR Am J Roentgenol. Mar 1993;160(3):593-600. [Medline].
• Schlaug G, Benfield A, Baird AE, et al. The ischemic penumbra: operationally defined by diffusion and perfusion MRI. Neurology. Oct 22 1999;53(7):1528-37. [Medline].
• Thurnher MM, Castillo M. Imaging in acute stroke. Eur Radiol. Mar 2005;15(3):408-15. [Medline].
• Yuh WT, Crain MR, Loes DJ, et al. MR imaging of cerebral ischemia: findings in the first 24 hours. AJNR Am J Neuroradiol. Jul-Aug 1991;12(4):621-9. [Medline].

Article Last Updated: Mar 13, 2007