Magnetic resonance imaging (MRI) is increasingly being used in the diagnosis and management of acute ischemic stroke and is sensitive and relatively specific in detecting changes that occur after such strokes.
Advances in MRI include 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. Recently, 7.0 and 9.4 T field strength MRI have been introduced with higher signal-to-noise (SNR) and contrast-to-noise (CNR) ratios compared to lower field strengths. However, limitations such as inhomogeneous transmit fields and extensive contraindications for patient scanning restricts their clinical application in acute stroke.
Inpatients may often continue to be monitored and receive treatment while undergoing MRI, because MRI-compatible electrocardiographic monitors, intravenous infusion pumps, and ventilators are available.
MRI has some limitations, such as high cost, long scanning duration, and decreased sensitivity in the detection of subarachnoid hemorrhages.
Go to Ischemic Stroke for more complete information on this topic.
Technological details
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 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 have demonstrated less spatial resolution than hydrogen. The 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).
The following are commonly used MRI techniques:
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 the 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
Patient education
For excellent patient education resources, visit eMedicineHealth's Brain and Nervous System Center. In addition, see eMedicineHealth's patient education articles Magnetic Resonance Imaging (MRI) and Stroke.
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 neuronal resting membrane potentials and the 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. Approximately 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 MRI scans 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.
Pacemakers, although new protocols allow imaging in selected cases
MR-incompatible prosthetic heart valves
Contrast allergy
Body weight (MRI tables have specific weight limitations)
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.
In the presence of any of these contraindications, a regular radiograph may be indicated.
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. (See the image below.)
View Image
The diffusion-weighted MRI reveals a region of hypointensity in the distribution of the right middle cerebral artery. Flanking the anterior and poster....
Numerous studies have shown that ADCs in ischemic areas are lower by 50% or more compared with those of normal brain areas, and they appear as bright areas (ie, hyperintensities) on DWI (see the image below). Studies have demonstrated that changes in the ADC occur as early as 10 minutes following the onset of ischemia.
View Image
Magnetic resonance imaging in acute stroke. Left: Diffusion-weighted MRI in acute ischemic stroke performed 35 minutes after symptom onset. Right: App....
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 symmetrical 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 the 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 have 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 the disappearance of the diffusion defect.
The technique most commonly used to acquire 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 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, studies have 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 University of North Carolina at Chapel Hill Stroke Center, 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 fluid-attenuated inversion recovery (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
T2 shine through - Associated with abnormal T2-WI and normal ADC map
With perfusion-weighted imaging (PWI), information about the perfusion status of the brain is available. The most commonly used technique is bolus-contrast tracking. 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.
Arterial spin-labeled (ASL) PWI permits noninvasive quantification of CBF without the use of contrast agent. There are two distinct forms of ASL that are used clinically: 1) continuous ASL (CASL) and 2) pseudocontinuous ASL (PCASL). A 2015 guideline paper outlines the methodological details of these individual techniques.[1]
The use of DWI and PWI together has been shown to be superior to the use of conventional MRI in early phases and up to 48 hours after the onset of stroke. Using a combination of DWI and PWI is very important, because together they provide information about the 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 and in predicting the outcome and prognosis.[2]
The lesion usually enlarges on serial DWI 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 (DPM), ie, the difference in size between lesions captured by DWI and PWI, usually represents the ischemic penumbra (see the image below), which is the region of incomplete ischemia that lies next to the core of the infarction.[3] The ischemic penumbra is regarded as an area that is viable but under ischemic threat.
View Image
Magnetic resonance imaging in acute stroke. Left: Perfusion-weighted MRI of a patient who presented 1 hour after onset of stroke symptoms. Right: Mean....
Drawbacks to diffusion-perfusion mismatch are mainly methodologic and include the following:
Lack of anatomic match between diffusion- and perfusion-weighted abnormality
Variable sensitivity of perfusion-weighted image based on Tmax delay
Visual versus quantitative estimation of mismatch
Recent trials (DEFUSE and EPIPHET) suggest that DPM is not an effective tool in selecting patients for intravenous tissue-type plasminogen activator (tPA [eg, alteplase]) beyond the traditional 3-hour window. The results of MR RESCUE suggest that DPM is not an effective tool to select patients for endovascular treatment of acute ischemic stroke. Thrombolysis and interventional stroke management in acute ischemic stroke has the benefit of promoting recanalization and improved neurological outcome. However, it also carries the risk of symptomatic intracerebral hemorrhage and possibly increased mortality. Criteria to diagnose DPM are still evolving. Validation of the mismatch selection paradigm is required with clinical trials. Pending these results, delayed treatment, even according to DPM selection, is not recommended.
One limitation of routine MR sequences (T1- and T2-weighted images) is in the 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. Recent guidelines suggest the use of CT or MRI to rule out hemorrhage prior to thrombolytic or interventional stroke management decisions. Due to the increased sensitivity of MR in detecting blood (acute as well as chronic), MRI may have the limitation of excluding patients who would otherwise be favorable treatment candidates.
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.
Blood oxygen level–dependent (BOLD) MRI is a technique that can be used to detect deoxyhemoglobin in the cerebral capillaries and veins as an MRI indicator of brain OEF.[4] Evidence suggests that BOLD MRI might provide a better estimation of the ischemic penumbra in acute ischemic stroke compared with MR diffusion-perfusion mismatch.
Resting state functional connectivity (FC) magnetic resonance imaging (MRI) (R-fMRI) measures, within a subject, the temporal correlation of the blood oxygenation level dependent (BOLD) signal across regions without any imposed task, providing a measure of temporal coherence of activity between brain regions. In a pilot study, we found that patients who received intravenous thrombolysis showed changes in resting state networks and functional outcomes over time. These findings point to an intriguing possibility that the improvement of resting state networks may reflect improved efficiency of brain activity that is potentially related to functional outcomes in acute stroke patients.[5]
Further validation of these techniques is required to confirm their clinical value in imaging of acute ischemic stroke.
Magnetic resonance spectroscopy (MRS) evaluates metabolic activity and the 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 neuron loss.
An increase in the lactate level is another important finding and has been attributed to anaerobic metabolism in ischemic tissue. Initial studies of other metabolites, such as choline and creatine, have 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 human and animal studies.
Long acquisition times, weak signal, and low spatial resolution associated with 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.
Magnetic resonance angiography (MRA) is very sensitive to flow and is based on the difference in signal between moving blood and stationary brain tissue; angiographic-like images of the cervicocranial vasculature are produced.
MRA images are a useful tool in identifying dissections, in that 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.
Three-dimensional time-of-flight MRA
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. In addition, 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 time-of-flight MRA
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. Their 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.
Phase-contrast MRA
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.
Thromboembolic infarction is the most common form of infarction. Typically, it is observed on MRI as a wedge-shaped infarct in the particular vascular distribution. Data support the hypothesis that a single infarct in a vascular territory is more likely to be thrombotic than are multiple infarcts, which are more likely to be embolic.
Watershed infarction occurs at the distal margins of specific arterial territories. It can occur superficially and can occur 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. Studies show that this type of infarction could be more readily detected by using DWI.
Lacunar infarctions
Lacunar infarctions 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 the basal ganglia, internal capsule, thalamus, brainstem, and cerebellum. MRI findings in these lesions follow the same pattern observed in thromboembolic infarction.
Cerebral vein and venous sinus occlusions
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 by 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 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.
Posterior reversible encephalopathy syndrome (PRES) presents clinically with acute/subacute onset headache, seizures, visual changes, altered mental status, and occasionally focal neurologic signs. MRI typically shows symmetrically distributed areas of vasogenic edema predominantly within the territories of the posterior circulation. The abnormalities affect primarily the white matter, but cortex is also involved. The diffusion weighted abnormality is associated with normal or high ADC value, differentiating the vasogenic edema induced by hypertension from cytoxic edema induced by ischemia.[6]
DWI is able to detect ischemic changes within minutes of onset (see the image below). Reduced proton motion is detected as a decreased ADC.
View Image
Magnetic resonance imaging in acute stroke. Left: Diffusion-weighted MRI in acute ischemic stroke performed 35 minutes after symptom onset. Right: App....
Early in the process of cerebral ischemia, PWI, using first-pass contrast bolus injection or spin tagging of the protons in the water in blood, reveals reductions in CBF and CBV and an increase in MTT of blood through the brain (see the image below).
View Image
Magnetic resonance imaging in acute stroke. Left: Perfusion-weighted MRI of a patient who presented 1 hour after onset of stroke symptoms. Right: Mean....
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 the image below).
View Image
Magnetic resonance imaging in acute stroke. Diffusion-perfusion mismatch in acute ischemic stroke. The perfusion abnormality (right) is larger than th....
A popular paradigm is to subject patients presenting beyond the 3-hour window to multimodal MRI to detect DPM; patients with mismatch may be candidates for stroke treatment. Two clinical trials have been completed that tested the hypothesis that patients with ischemic penumbra as detected by DPM mismatch may benefit from thrombolysis beyond the 3-hour treatment window.
Both studies seemed to show lack of benefit, suggesting that patients selected based on DWI/PWI mismatch do not benefit from intravenous thrombolysis beyond the 3-hour window. Both the studies, the EPITHET and the DEFUSE trials, randomized patients presenting 3-6 hours with greater than 20% DWI/PWI mismatch to intravenous tissue-type plasminogen activator (tPA) or placebo.[7] The ECASS-3 trial did not use such an MRI paradigm and has shown benefit of intravenous tPA in acute ischemic stroke 3-4.5 hours from onset.[8]
These trials raise several technical issues with DWI/PWI mismatch, particularly with regard to (1) most appropriate DWI/PWI ratio, (2) the most appropriate PWI threshold, (3) the coregistration of DWI and PWI, and (4) the online automated assessment of mismatch. EPIPHET and DEFUSE failed to show the utility of DPM in selecting patients for IV tPA beyond the traditional 3-hour window.[7] The MR RESCUE similarly showed that DPM was not a useful tool in selecting patients who may benefit from interventional stroke management.[9]
Newer MRI techniques are being developed to assess regions of reversible ischemia. Susceptibility-weighted imaging, such as BOLD functional MRI (BOLD-fMRI), is considered to provide a surrogate for brain OEF measurement and is one such emerging technique.[10]
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-weighted imaging (T2-WI). At 2-4 hours, T1-weighted imaging (T1-WI) shows subtle effacement of the sulci due to cytotoxic edema. At 8 hours, T2-WI shows hyperintense signal due to cytotoxic and vasogenic edema. At 16-24 hours, T1-WI shows hypointense signal due to cytotoxic and vasogenic edema.
Contrast-enhanced images show arterial enhancement followed by parenchymal enhancement. The arterial enhancement can be very early (in >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 gradient-recalled echo (GRE) sequence.
MRI findings arising from acute ischemic changes are summarized in the table below.
Table. MRI Findings in Acute Ischemic Changes
View Table
See Table
Acute phase (1-7 d)
In this phase, edema increases, maximizing at 48-72 hours, 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. In addition, 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 petechial and frank hemorrhages 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 T1-WI and T2-WI.
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.
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 also persists throughout this phase; it usually disappears by 3-4 months.
Following acute ischemic stroke, treatment measures to induce reperfusion must be implemented within a recognized time frame ,which means that timely recognition of this condition is vital. This involves bedside assessments followed by appropriate imaging studies including MRI. Stroke mimics including metabolic, traumatic, migranous, neoplastic, convulsive, and psychiatric disorders account for 3-30% of patients presenting with acute neurological deficits.[11] A rapid MRI sequence may be used to select patients for rapid diagnosis and treatment.[12] Such MRI sequence typically incorporates diffusion weighted sequence, FLAIR and gradient sequence, requiring less than 10 minutes, and have been successfully incorporated into acute stroke management protocol.
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.
Although TIAs have been traditionally defined as transient (< 24 h) neurologic deficits of vascular origin, the advent of MRI has led to reconsideration of the definition. Recent tissue definitions of stroke emphasize that TIA with persistent ischemia on diffusion-weighted imaging is classified as stroke rather than a TIA. TIA, on the other hand, requires either a normal diffusion-weighted image without evidence of ischemia or reversible changes on DWI suggestive of ischemia rather than infarction.[13]
Recently, brain imaging (DWI) has been added to the clinical ABCD2 to identify patients with TIA with a high risk of stroke recurrence. The ABCD3-I score uses DWI and intracranial atherosclerosis detected by MRA to add prognostic value to the traditional ABCD2 score. It appears that DWI abnormality increases the ability to predict stroke at 7 and 90 days in patients presenting with clinical TIA. Intracranial disease on MRA seems to add to this score in a nonsignificant way.[14]
Go to Transient Ischemic Attack for more complete information on this topic.
GRE and EPI sequences have the ability to detect microbleeds that are clinically silent and not visualized by computed tomography (CT) scanning or routine MRI 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.[15]
GRE, EPI, and DWI (B0) are sensitive in 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). However, the current guidelines do not advocate the use of MRI in place of CT scanning to screen patients for thrombolysis.
Go to Hemorrhagic Stroke for more complete information on this topic.
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-, diffusion-, or perfusion-weighted imaging and MRA. Many institutions have established acute stroke protocols to minimize scanning time.
The 2013 guidelines for early management of acute ischemic stroke recommend that although in most instances CT provides the necessary information, MRI may be used before intravenous TPA administration to exclude ICH (absolute contraindication) and to determine whether MRI hyperintensity of ischemia is present (Class I; Level of Evidence A).[16]
What is the role of MRI in the diagnosis and management of acute stroke?Which MRI techniques are used in the diagnosis and management of acute stroke?What is the pathogenesis of MRI findings in acute stroke?What are contraindications for MRI in the diagnosis and management of acute stroke?What is the role of diffusion-weighted imaging (DWI) in the workup of acute stroke?Which findings on diffusion-weighted imaging (DWI) suggest acute stroke?How are other conditions with areas of hyperintensity on diffusion-weighted imaging differentiated from acute stroke?What is the role of perfusion-weighted imaging (PWI) in the workup of acute stroke?What is the role of diffusion-perfusion mismatch (DPM) in acute stroke imaging?What is the role of blood oxygen level-dependent (BOLD) MRI in acute stroke imaging?What is the role of echo-planar imaging in the workup of acute stroke?What is the role of MRA in the workup of acute stroke?What is the role of 3D time-of-flight (TOF) MRA in acute stroke imaging?What is the role of 2D time-of-flight (TOF) MRA in acute stroke imaging?What is the role of phase-contrast MRA in acute stroke imaging?Which MRI findings are characteristic of thromboembolic infarction in the workup of acute stroke?Which MRI findings are characteristic of lacunar infarction in in the workup of acute stroke?Which MRI findings are characteristic of cerebral vein and venous sinus occlusions in the workup of acute stroke?Which MRI findings are characteristic of posterior reversible encephalopathy syndrome (PRES) in the workup of acute stroke?Which MRI findings are characteristic of the hyperacute phase (0-24 h) of acute stroke?Which MRI findings are characteristic of the acute phase (1-7 d) of acute stroke?Which MRI findings are characteristic of the subacute phase (7-21 d) of acute stroke?Which MRI findings are characteristic of the chronic phase (>21 d) of acute stroke?What is the role of rapid MRI in the diagnosis of acute stroke?What are the MRI findings characteristic of TIA?What is the role of MRI in the workup of hemorrhagic stroke?When is minimized MRI scanning time indicated in the workup of acute stroke?What are the AHA/ASA guidelines on use of MRI in the early management of acute stroke?
Souvik Sen, MD, MPH, MS, FAHA, Professor and Chair, Department of Neurology, University of South Carolina School of Medicine
Disclosure: Nothing to disclose.
Coauthor(s)
Amar Anand, MD, Resident Physician, Department of Neurology, Palmetto Health, Medical University of South Carolina College of Medicine
Disclosure: Nothing to disclose.
Chief Editor
Helmi L Lutsep, MD, Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center
Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2; Physician Advisory Board for Coherex Medical; National Leader and Steering Committee Clinical Trial, Bristol Myers Squibb; Consultant, Abbott Vascular, Inc. .
Acknowledgements
Draga Jichici, MD, FRCP, FAHA Associate Clinical Professor, Department of Neurology and Critical Care Medicine, McMaster University School of Medicine, Canada
Draga Jichici, MD, FRCP, FAHA is a member of the following medical societies: American Academy of Neurology, Canadian Congress of Neurological Sciences, Canadian Congress of Neurological Sciences, Canadian Congress of Neurological Sciences, Canadian Critical Care Society, Canadian Medical Protective Association, Canadian Neurocritical Care Society, Neurocritical Care Society, Royal College of Physicians and Surgeons of Canada, and Society of Critical Care Medicine (USA)
Disclosure: Nothing to disclose.
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: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
){kind=link}
){kind=link}
){kind=link}
){kind=link}