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Figure 3 Acute ischemia; MR techniques compared. Two hours after stroke, the T2-weighted MR (left) may be completely normal. Fluid attenuation inversion recovery (FLAIR) imaging may reveal hyperintense vessels in the region of the infarction (arrow). The diffusion weighted image (DWI) reveals an area of infarction (as shown in Fig. 2). Perfusion weighted imaging (PWI) shows a large area of diminished perfusion that has not yet become infarcted, as shown by the discrepancy between the DWI and the PWI. This "mismatch" corresponds to a large area of brain tissue that is potentially at risk for infarction [adapted with permission from R. Bakshi and L. Ketonen, Brain MRI in clinical neurology. In Baker's Clinical Neurology (R. J. Joynt and R. C. Griggs, Eds.). Copyright Lippincott, Williams & Wilkins, 2001].

Figure 4 Acute hemorrhage seen on MR. This is a T1-weighted MR, without contrast, demonstrating hemorrhagic transformation within a large middle cerebral artery stroke within 7 days following the stroke [adapted with permission from R. Bakshi and L. Ketonen, Brain MRI in clinical neurology. In Baker's Clinical Neurology (R. J. Joynt and R. C. Griggs, Eds.). Copyright Lippincott, Williams & Wilkins, 2001].

Figure 4 Acute hemorrhage seen on MR. This is a T1-weighted MR, without contrast, demonstrating hemorrhagic transformation within a large middle cerebral artery stroke within 7 days following the stroke [adapted with permission from R. Bakshi and L. Ketonen, Brain MRI in clinical neurology. In Baker's Clinical Neurology (R. J. Joynt and R. C. Griggs, Eds.). Copyright Lippincott, Williams & Wilkins, 2001].

surrounding tissues. By 16-24 hr following ischemic infarction, there is usually enough vasogenic edema to cause T1 signal hypointensity. Within 5-7 days after ischemic infarction, there is parenchymal enhancement following injection of gadopentate dimeglumine. The new blood vessels that form within damaged areas surrounding a complete infarction have an imperfect blood-brain barrier, allowing contrast to leak into surrounding tissues.

Hemorrhages may be evident on MRI, but the time course and evolution are much more complex than with ischemic infarction. For example, subarachnoid or intraventricular hemorrhages evolve differently than subdural or epidural hematomas. Intraparench-ymal hematomas are different as well. FLAIR images enable detection of oxygenated hemoglobin in acute subarachnoid hemorrhage, and the superiority of CT scanning for the purpose of acute detection of subarachnoid hemorrhage has thus been challenged. Acute intraparenchymal hemorrhages may be missed by T1, T2, and proton density images; these techniques do not show alteration in signal intensity (i.e., decreases) for 1-3 days due to the gradual accumula tion of deoxygenated hemoglobin. As red blood cells degrade, deoxygenated hemoglobin is converted to met-hemoglobin, which may appear hyperintense on T1 images 3-7 days after a hemorrhage. There is gradual accumulation of hemosiderin as the breakdown of hemoglobin continues from 1 to 4 weeks. Met-hemoglobin is typically hyperintense on T1, T2, and proton density images, whereas hemosiderin (which accumulates after 4 weeks) produces low signal intensities on T1, T2, and proton density images. Figs. 7 and 8 illustrate the typical progression of brain hemorrhage seen with MR techniques.

MR techniques are important for visualizing the arteries supplying the brain. MRA allows the visualization of intracranial and extracranial arteries of medium and large caliber. Turbulent flow will produce flow signal dropout, which may lead to false interpretations of vessel occlusion. Even relatively large aneurysms may be missed with MRA, and the technique has not yet replaced catheter angiography as the gold standard for defining cerebrovascular anatomy. MRV is sensitive to blood flowing at slower velocities, such as the blood within cerebral veins and sinuses. MRV is thus an important tool for detecting sagittal sinus thrombosis, cortical vein thrombosis, and other disorders of the cerebral veins.

Perfusion imaging (T2*) allows qualitative evaluation of CBF. Areas of relatively reduced CBF can be identified, and a "diffusion-perfusion mismatch'' may indicate a large area of brain in danger of complete infarction (Fig. 3). Changes in CBF are being utilized to map the parts of the brain that participate in various kinds of neurological or cognitive functions. Functional MRI (fMRI) may soon become an essential part of the management of cerebrovascular disorders. Not only will it enable detection of diffusion-perfusion mismatch in acute stroke patients eligible for intravenous or intraarterial thrombolysis but also fMRI may facilitate appropriate selection of arteries that might safely be sacrificed in the management of arteriove-nous malformation. Magnetic resonance spectroscopy (MRS) allows the breakdown products of tissue destruction to be measured quantitatively. Thus, MRS may become an important method of detecting the presence of injury or measuring the effect of neuroprotective interventions. Its use in clinical practice is currently limited.

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