Table III

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Neuroimaging Techniques"


Transcranial Doppler Volume flow imaging B-mode M-mode Computed tomography Without contrast With contrast CT angiography CT perfusion (e.g., Xe) Magnetic resonance T1 weighted T2 weighted Proton density FLAIR MRA MRV DWI PWI


Others (magnetization transfer, gradient echo, ADC, etc.) SPECT HMPAO 133Xe PET 15O CBF


"Note that some neuroimaging techniques (e.g., PET) are not commonly used for clinical purposes. There are several new neurosonology and magnetic resonance imaging techniques (see text for details) not listed in the table. CT, computed tomography; MR, magnetic resonance; MRA, MR angiography; MRV, MR venography; FLAIR, fluid attenuation inversion recovery; SPECT, single photon emission computed tomography; CBF, cerebral blood flow; HMPAO, [99mTc]d,1-hexamethylpropylene amine oxime; DWI, diffusion weighted imaging; PWI, perfusion weighted imaging; and ADC, apparent diffusion coefficient.

evidence of arterial narrowing predisposing to later stroke), during the acute stages of stroke (e.g., to identify viable brain tissue at risk for infarction that may be salvaged by intraarterial or intravenous thrombolysis, as in Fig. 3), and following a cerebrovascular diagnosis (e.g., to clarify whether a hemor-rhagic area was really due to stroke rather than hemorrhage into a rapidly growing brain tumor). These benefits are achieved without undue risks; the presence of a cardiac pacemaker, brain aneurysm clip, or the presence of other metallic foreign bodies (e.g., metal in the eye) are the only contraindications to brain MR. MR is useful in the imaging of both ischemic and hemorrhagic processes (Figs. 3-5).

The earliest sign of ischemic infarction apparent on MR is the loss of the normal intravascular "flow void'' due to slow flow or occlusion within an intracranial vessel. This finding is similar to the "dense MCA sign'' described in CT images of acute stroke. Arterial hyperintensity may be apparent on fluid attenuation inversion recovery (FLAIR) images almost immediately after stroke. Venous hyperintensity on FLAIR imaging suggests venous thrombosis, which may be confirmed with MRV (Fig. 6). Two to 4 hr following acute ischemic infarction, subtle changes in the shape of cortical gyri may become evident due to cytotoxic edema, which causes neural tissue to swell. Diffusion weighted MR reveals abnormalities within 30 min of acute ischemic infarction and is rapidly becoming a valuable technique for acute stroke imaging (Figs. 2 and 3). The majority of acute ischemic infarcts can be identified using diffusion MR, which reportedly detects 97% while remaining normal in 100% of individuals lacking acute ischemic infarction. Signal hyperintensity on T2 and proton density images becomes apparent within 8 hr of an ischemic infarction as a result of vasogenic edema, the process whereby water extravasates from damaged vessels into the

Diffusion-Perfusion: stroke at 2h m

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