Recently, several implementations of arterial spin labeling (ASL) techniques have been developed for producing MRI images sensitive to local tissue perfusion. For quantitation of perfusion, both pulsed and continuous labeling methods potentially suffer from a number of systematic errors. In this study, a general kinetic model for the ASL signal is described that can be used to assess these errors. With appropriate assumptions, the general model reduces to models that have been used previously to analyze ASL data, but the general model also provides a way to analyze the errors that result if these assumptions are not accurate. The model was used for an initial assessment of systematic errors due to the effects of variable transit delays from the tagging band to the imaging voxel, the effects of capillary/tissue exchange of water on the relaxation of the tag, and the effects of incomplete water extraction. In preliminary experiments with a human subject, the model provided a good description of pulsed ASL data during a simple sensorimotor activation task.

Our purpose was to use whole brain echo planar magnetic resonance imaging (MRI) to identify and characterize diffusion abnormalities in acute cerebral ischemia. We studied 40 patients as early as 3 hours after onset of signs and symptoms of cerebral ischemia. Diffusion-weighted imaging (DWI) of the entire brain could be completed in 3 seconds or, using seven different diffusion sensitivities (maximum b = 1,271 sec/mm2), in 48 seconds. Measurements and synthetic maps were made of apparent diffusion coefficients (ADC), a physiological parameter that characterizes the self-diffusion of water in tissue. Early ischemic lesions were identified with DWI as hyperintense regions of decreased ADC in all patients who subsequently developed infarction, before changes were evident on conventional MRI in cases studied earlier than 6 hours after onset of ischemic symptoms. Lesions as small as 4 mm in diameter were identified. The extent of lesions within white matter was best defined by controlling for the anisotropic effect of axonal orientation. The mean ADC (+/- SD) for control regions in the 36 patients was 9.15 (+/- 2.91) x 10(-4) mm2/sec. Mean ADC of ischemic regions was 56% of control values at 6 hours or less and stayed significantly reduced for 3 to 4 days after onset of ischemia. The relative ADC increased progressively over time to be pseudonormalized at 5 to 10 days and elevated in the chronic state, making the distinction of acute lesions adjacent to chronic infarcts readily apparent. DWI with echo planar imaging measures a unique physiological parameter that is sensitive to ischemic changes before conventional MRI. Its potential role in the quantitative study of human stroke pathophysiology and therapeutics is the subject of further investigation.

These MR indexes may allow the identification and quantification of viable but ischemically threatened cerebral tissue amenable to therapeutic interventions in the hyperacute care of stroke patients.

Rapid MRI of the molecular diffusion of water demonstrated cerebral infarcts in 32 patients. We studied these patients at various times following the onset of ischemic symptoms and found that diffusion-weighted imaging revealed the infarcts sooner than conventional T2-weighted spin-echo imaging did; four hyperacute infarcts were shown only by diffusion-weighted imaging. Acute infarcts had lower apparent diffusion coefficients (ADCs) than noninfarcted regions did. This relative difference in ADC reached a nadir in the first 24 hours and rose progressively thereafter. Chronic infarcts showed a relative increase in diffusion and were readily distinguishable from acute infarcts. The technique takes less than 2 minutes to apply using a standard 1.5-tesla scanner in the clinical setting. Diffusion-weighted imaging has the potential to play a role in improving the early anatomic diagnosis of stroke and therefore in the development and implementation of early stroke interventions.

The EPISTAR technique is a rapid, noninvasive means for creating qualitative maps of CBF.

We aimed to determine the frequency and time course of the enlargement of ischemic cerebral lesions following human stroke and to study the effect of the state of perfusion on lesion enlargement. Acute lesion volumes were measured on diffusion-weighted magnetic resonance images and compared with lesion volumes measured on T2-weighted images at 7 days or later. Forty-four measurements were performed between 2 and 53 hours after stroke onset in 28 patients. Thirteen patients also had magnetic resonance perfusion imaging performed. In 12 (43%) of 28 patients the initial lesion volume increased by 20% or more. The number of studies showing enlargement of the ischemic lesion volume ranged from 12 (43%) of 28 at or after 2 hours to 10 (38%) of 26 at or after 6 hours, 5 (33%) of 15 at or after 24 hours, and 2 (33%) of 6 at or after 48 hours. In 7 of the 10 patients in whom the hypoperfusion volume acutely exceeded the volume of the abnormality on diffusion-weighted images, lesion volume increased by 20% or more. This study provided evidence that substantial enlargement of human cerebral ischemic lesion volumes can occur beyond the first 6, 12, or 24 hours after onset. A mismatch acutely between the region of hypoperfusion (larger) and the region of diffusion abnormality (smaller) may be predictive of ischemic lesion enlargement.

BOLD MRI can be used to monitor changes in intrarenal oxygenation in humans in a noninvasive fashion.

Diffusion-weighted MRI can rapidly detect acute cerebral ischemic injury as hyperintense signal changes, reflecting a decline in the apparent diffusion coefficient (ADC) of water through brain parenchyma, whereas ADC is elevated in the chronic stage because of increased extracellular water content. To determine the time course of these ADC changes, we analyzed 157 diffusion-weighted MRI studies performed at varying time points from the initial ischemic event from 101 patients. Data were expressed as the relative ADC (rADC), the ratio of lesion to control regions of interest. We observed two phases in the time course of rADC changes in acute human stroke: a significant (p < 0.005) reduction in rADC lasting for at least 96 hours from stroke onset (mean, 58.3% of control; SEM, 1.47) and an increasing trend from reduction to pseudonormalization to elevation of rADC values at later subacute to chronic time points (> or = 7 days). We suggest that the persistent reduction of rADC within the first four days may reflect ongoing or progressive cytotoxic edema to a greater degree than extracellular edema and cell lysis.