Sodium imaging intensity increases with time after human ischemic stroke.

OBJECTIVE: Establishing time of onset is important in acute stroke management. Current imaging modalities do not allow determination of stroke onset time. Although correlations between sodium magnetic resonance imaging signal intensity within ischemic lesions and time of onset have been shown in animal models, the relation to onset time has not been established in human stroke. Utilizing high-quality sodium images, we tested the hypothesis that sodium signal intensity increases with time from symptom onset in human ischemic stroke. METHODS: Twenty-one stroke patients (63 +/- 15 years old) were scanned 4 to 104 hours after symptom onset. Follow-up images were obtained in 10 patients at 23 to 161 hours after onset, yielding a total of 32 time points. A standard stroke imaging protocol was acquired at 1.5 Tesla, followed by sodium magnetic resonance imaging at 4.7 Tesla. Relative sodium signal intensity within each lesion was measured with respect to the contralateral side. RESULTS: The sodium image quality was sufficient to visualize each acute lesion (lesion volume range, 1.7-217cm(3)). Relative sodium signal intensity increased nonlinearly over time after stroke onset. Sodium images acquired within 7 hours (n = 5) demonstrated a relative increase in lesion intensity of 10% or less, whereas the majority beyond 9 hours demonstrated increases of 23% or more, with an eventual leveling at 69 +/- 18%. INTERPRETATION: Increases of sodium signal intensity within the ischemic lesion are related to time after stroke onset. Thus, noninvasive imaging of sodium may be a novel metabolic biomarker related to stroke progression. Ann Neurol 2009;66:55-62.

Elevations of diffusion anisotropy are associated with hyper-acute stroke: a serial imaging study.

Diffusion tensor imaging (DTI) studies of human ischemic stroke within 24 h of symptom onset have reported variable findings of changes in diffusion anisotropy. Serial DTI within 24 h may clarify these heterogeneous results. We characterized longitudinal changes of diffusion anisotropy by analyzing discrete ischemic white matter (WM) and gray matter (GM) regions during the hyperacute (2.5-7 h) and acute (21.5-29 h) scanning phases of ischemic stroke onset in 13 patients. Mean diffusivity (MD), fractional anisotropy (FA) and T2-weighted signal intensity were measured for deep and subcortical WM and deep and cortical GM areas in lesions outlined by a > or =30% decrease in MD. Average reductions of approximately 40% in relative (r) MD were observed in all four brain regions during both the hyperacute and acute phases post stroke. Overall, 9 of 13 patients within 7 h post symptom onset showed elevated FA in at least one of the four tissues, and within the same cohort, 11 of 13 patients showed reduced FA in at least one of the ischemic WM and GM regions at 21.5-29 h after stroke. The fractional anisotropy in the lesion relative to the contralateral side (rFA, mean+/-S.D.) was significantly elevated in some patients in the deep WM (1.10+/-0.11, n=4), subcortical WM (1.13+/-0.14, n=4), deep GM (1.07+/-0.06, n=1) and cortical GM (1.22+/-0.13, n=5) hyperacutely (< or =7 h); however, reductions of rFA at approximately 24 h post stroke were more consistent (rFA= 0.85+/-0.12).