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We image patients with stroke syndromes to establish a diagnosis and to guide patient management, especially when there is a reasonable likelihood of intervention improving outcomes. Computed tomography (CT)- and magnetic resonance imaging (MRI)-based imaging, often in combination, are commonly used. With recent major advances in the treatment of the severe ischemic stroke caused by occlusions of the major cerebral arteries, a critical assessment is underway on how to optimize triage decisions to deliver the best care. The most important clinical and physiological determinants of patient outcomes include: severity of the neurological deficit, site of arterial occlusion, size of the infarct core as a function of the collateral circulation, and the success of recanalization. Imaging provides essential physiological information, but time is required. Thus a tension exists between obtaining most precise physiological information and the need to restore cerebral perfusion as soon as possible. This chapter focuses on how the use of MR results in optimal outcomes in patients undergoing endovascular intervention even outside the traditional time windows. Of course, MR is just as valuable in evaluating patients with all types of ischemic strokes and TIAs, because it is superior to all other imaging methods in revealing stroke physiology. While the focus here is on imaging the acute stroke patient, the basic MRI principles are applicable to all stroke and transient ischemic attack (TIA) patients. These basic principles are described here, without detailed documentation. The reader interested in the documentation is directed to the bibliography at the end, particularly the relevant chapters in the book from which this contribution is in part derived.
MR has greatly enhanced our understanding of ischemic stroke. It is a widely available and practical clinical tool, and is commonly employed to diagnose and guide the treatment of acute stroke patients. It is particularly useful in patients with major stroke syndromes caused by the occlusions of major arteries of the anterior circulation, because it is the most precise method to select patients that are most likely to benefit from endovascular thrombectomy. What follows is an overview of the MR methods most useful in evaluating the patient with ischemic stroke.
Diffusion MRI, commonly designated DWI (diffusion-weighted imaging), is highly sensitive and specific in the detection of acute ischemic stroke at early time points when CT and conventional MR sequences are unreliable . The initial DWI lesion is a marker of severe ischemia and progresses to infarction unless there is early reperfusion. The initial diffusion lesion volume correlates highly with final infarct volume as well as with acute and chronic neurologic assessment. Conventional CT and MRI cannot reliably detect infarction at early time points. Sensitivities are less than 50% for these modalities within 6 h of ictus. The sensitivity and specificity for DWI are in the upper 90% range .
Contrast mechanisms . Acute ischemia results in reduction in tissue water diffusivity, and is the principal source of lesion detection by DWI. The biophysical basis for this change is complex and not fully understood. Mechanisms include: failure of ionic pumps with net transfer of water from the extracellular to the intracellular compartment; reduced extracellular space volume and increased tortuosity of extracellular space pathways; increased intracellular viscosity from microtubule dissociation and fragmentation of other cellular components; increased intracellular space tortuosity; decreased cytoplasmic mobility; temperature decrease; and increased cell membrane permeability.
Time course . In rodent studies, experimental middle cerebral artery (MCA) occlusion is followed by a decline in water diffusivity as early as 10 min after occlusion. Diffusion coefficients pseudonormalize at about 48 h, and are elevated thereafter. In humans, decreased diffusion in ischemic brain tissue has been reported as early as 11 min after vascular occlusion. The apparent diffusion coefficient (ADC) continues to decrease with maximum reduction at 1–4 days. This decreased diffusion appears hyperintense on DWI (which combines T2 and diffusion weighting) and hypointense on ADC images. The ADC returns to baseline at 1–2 weeks. At this point, the infarct appears mildly hyperintense on the DWI images and isointense on the ADC images. Thereafter, while the DWI can be variable (slight hypointensity, isointensity, or hyperintensity, depending on the relative strength of the T2 versus diffusion components), the ADC is elevated because of increased water content of encephalomalacic tissue. The time course is influenced by a number of factors including infarct type and size, as well as patient age .
Reversibility . In the vast majority of stroke patients, the DWI abnormality represents tissue that is destined to infarct. The final infarct volume usually includes the initial DWI lesion and other surrounding tissue into which the infarct extends. However, at least partial DWI reversal following early reperfusion is observed. Studies in nonhuman primates have shown that temporary occlusions of cerebral arteries of less than an hour commonly result in true DWI reversal, while occlusions of 3 h or more followed by reperfusion produces a temporary pseudonormalization. Reversibility is variable with temporary occlusions of between 1 and 3 h. This is similar to the experience in human stroke. After 3 h of cerebral artery occlusion, the DWI abnormality represents irreversibly injured tissue regardless of the pseudonormalization that may be seen after reperfusion.
Sequences that are sensitive to local disturbances in the magnetic field permit identification of blood products including thrombus that causes vascular occlusion, parenchymal hematoma, and chronic microhemorrhages. Such blood products produce hypointensities on T2∗-weighted images created using gradient recalled echo sequences or can detect intraluminal thrombus (due to its high content of paramagnetic deoxyhemoglobin) in hyperacute infarcts as a linear low signal region of magnetic susceptibility. Susceptibility-weighted imaging (SWI) is a type of T2∗-weighted imaging that utilizes both phase and magnitude information obtained from high-resolution 3D gradient echo-based sequences, which produces images that accentuate differences in magnetic susceptibility. SWI also demonstrates decreased signal in veins in regions with reduced perfusion due to the increase in intravascular deoxyhemoglobin.
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