Magnetic Resonance Imaging in Stroke

Magnetic resonance imaging (MRI) provides non-invasive information about the brain’s blood flow, water movement and biochemical abnormalities following stroke, and advances in MRI are transforming the investigation and treatment of cerebrovascular disease. Echoplanar techniques with diffusion- and perfusion-weighted imaging, together with developments in magnetic resonance spectroscopy and angiography, are replacing CT scanning as the diagnostic modality of choice. In this profusely illustrated book, world leaders in these technologies review the scientific basis and clinical applications of MRI in stroke. It will appeal to a broad readership including stroke physicians, neurologists, neurosurgeons, rehabilitation specialists, and others with a clinical or research interest in cerebrovascular disease.
MRI is supremely sensitive to the abnormal accumulation of water, much more so than is CT, so it might be expected that MRI is superior to CT in the detection of ischemic infarction. Although this principle is applicable to subacute infarction, it is not the case in the first 6 hours after the onset of the ischemic insult. A basic understanding of the pathological processes which precede infarction is necessary in order to understand their MRI manifestations.
Pathology of ischemic infarction
Deprivation of oxygen supply to neurones, whether as a result of embolus, thrombosis or prolonged hypotension, leads initially to malfunction in as little as a few seconds, e.g. a Stokes–Adams attack, in which brainstem ischemia induces unconsciousness within seconds of cardiac asystole. If the
ischemic insult is prolonged the highly energy dependent sodium pump mechanism, which is responsible for maintaining a tenfold difference in extracellular to intracellular sodium concentration, begins to fail and sodium, water and calcium ions pass from the extracellular to the intracellular
space. The cell swells, producing ‘cytotoxic’ edema and the extracellular space is simultaneously reduced. If the diminished oxygen supply is maintained, the less energy-dependent capillary endothelial cells start to lose their function and the normally tight junctions between them begin to lose their integrity. Intravascular fluid leaks into the extravascular space, producing ‘vasogenic’ edema. Vasogenic edema spreads easily through the white matter due to its relatively less dense cellular density and more capacious extravascular space. The process of cytotoxic edema predominates in the first 6–8 hours. Subsequently, vasogenic edema becomes progressively more dominant and is largely responsible for the brain swelling in the first few days after the onset of infarction.
MRI technique
The basic standard MRI sequences which should be applied in screening for stroke are T1 and T2- weighted axial or sagittal scans through the whole
brain. The type of T2-weighted scans used is important. Conventional T2-weighted spin echo sequences allow the acquisition of minimally T2-weighted images or proton-weighted images as the first echo of a double echo sequence. Images acquired from the second echo of the spin echo sequence will be both heavily T2-weighted and sensitive to the magnetic susceptibility effects of ferromagnetic blood products such as deoxyhemoglobin, intracellular methemoglobin and hemosiderin. The T2-weighted multiple spin echo sequences used most commonly include ‘fast spin echo’, ‘turbo spin echo’ and ‘rapid spin echo’. Although they provide exquisite T2 weighting and spatial resolution, they suffer in that they are relatively insensitive to magnetic susceptibility effects and, hence, to hemorrhage. In the stroke context that is unacceptable. Therefore if one of these techniques is used, a further T2-weighted magnetic susceptibility sensitive technique should be added. Appropriate sequences include echoplanar imaging spin echo (EPI SE) or T2-weighted gradient echo
(GE). A very appropriate substitute for protonweighted sequences is fluid attenuated inversion recovery (FLAIR). While retaining heavy T2-weighting the cerebrospinal fluid is nulled, making any parenchymal abnormality more conspicuous. Furthermore, FLAIR sequences have been reported to be the only MRI sequence with high sensitivity and specificity in the detection of acute subarachnoid hemorrhage1 and to be able to detect vessel occlusion and perfusion deficits more sensitively than conventional spin echo sequences2,3. FLAIR’s drawback is its relative insensitivity to infratentorial intraaxial lesions.
In hyperacute stroke MRA sequences provide valuable and accurate information in respect to the patency of the major intracranial vessels. A rapid phase contrast MRA sequence can be obtained in restless patients in less than 2 minutes, while a more detailed time of flight (TOF) study of the intracranial circulation can be obtained in more cooperative patients. Diffusion-weighted imaging (DWI), when available, should be a mandatory sequence in any protocol for stroke evaluation.
Right middle cerebral artery territory infarct at 6 hours. T1 and T2-weighted scans through vertex (a), (b) show swollen right precentral and postcentral gyri, but no intrinsic signal abnormality. T1-weighted post contrast scan (c) shows stasis in precentral and central arteries and pial enhancement from leptomeningeal collateral feeders.
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