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Background and Purpose— Lacunar stroke is associated with endothelial dysfunction and histologically with intrinsic cerebral microvascular disease of unknown cause. Endothelial dysfunction could impair blood–brain barrier integrity. We assessed background blood–brain barrier leakage in patients with lacunar ischemic stroke compared with cortical stroke controls. Methods— We recruited patients with lacunar or mild cortical ischemic stroke and assessed generalized cerebral blood–brain barrier leak with MRI and intravenous gadolinium at least 1 month after stroke. We used detailed image processing to compare signal change before and for 30 minutes postcontrast throughout gray matter, white matter, and cerebrospinal fluid with summary analyses and general linear modeling. Results— Among 48 patients (29 lacunar, 19 cortical), postcontrast enhancement was significantly higher in cerebrospinal fluid ( P =0.04, Mann-Whitney U ), and nonsignificantly higher in white matter, in lacunar than in cortical strokes, with no difference in gray matter. General linear modeling confirmed significantly greater postcontrast enhancement in cerebrospinal fluid in lacunar patients than in cortical controls ( t =3.37, P Conclusion— These preliminary data suggest that the blood–brain barrier may be dysfunctional throughout subcortical white matter (white matter drains via interstitial spaces to cerebrospinal fluid) in patients with lacunar stroke. Further studies are required to confirm these findings and determine whether abnormal blood–brain barrier might predate development of lacunar disease. Blood–brain barrier dysfunction may be an important mechanism for brain damage in cerebral microvascular disease.

Background and Purpose— Some infarcts have persistently hyperintense areas on diffusion-weighted MRI (DWI) even at 1 month after stroke, whereas others have become isointense to normal brain. We hypothesized that late DWI hyperintensity reflected different infarct evolution compared with areas that were isointense by 1 month. Methods— We recruited patients prospectively with ischemic stroke, performed DWI and perfusion-weighted MRI (PWI) on admission, at 5 days, 14 days, and 1 month after stroke, and assessed functional outcome at 3 months (Rankin Scale). Patient characteristics and DWI/PWI values were compared for patients with or without “still hyperintense” infarct areas on 1-month DWI. Results— Among 42 patients, 27 (64%) had “still hyperintense” infarct regions at 1 month, mostly in white matter. Patients with “still hyperintense” regions at 1 month had lower baseline apparent diffusion coefficient ratio (ADCr; mean±SD 0.76±0.12 versus 0.85±0.12; hyperintense versus isointense; P P P P Conclusion— The late DWI lesion hyperintensity emphasizes the heterogeneity in temporal evolution of stroke injury and suggests ongoing “ischemia.” Lower baseline ADCr precedes delayed perfusion normalization, suggesting that worse cell swelling impedes reperfusion. Further study is required to determine underlying mechanisms and any potential for subacute intervention to improve recovery.

Background and Purpose— An acute mismatch on diffusion-weighted MRI (DWI) and perfusion-weighted MRI (PWI) may represent the “tissue-at-risk.” It is unclear which “semiquantitative” perfusion parameter most closely identifies final infarct volume. Methods— Acute stroke patients underwent DWI and PWI (dynamic-susceptibility contrast imaging) on admission (baseline), and T 2 -weighted imaging (T 2 WI) at 1 or 3 months after stroke. “Semiquantitative” mean transit time (MTT sq =first moment of concentration/time curve), cerebral blood volume (CBV sq =area under concentration/time curve), and cerebral blood flow (CBF sq =CBV sq /MTT sq ) were calculated. DWI and PWI lesions were measured at baseline and final infarct volume on T 2 WI acquired ≥1 month after stroke. Baseline DWI, CBF sq , and MTT sq lesion volumes were compared with final T 2 WI lesion volume. Results— Among 46 patients, baseline DWI and CBF sq lesions were not significantly different from final T 2 WI lesion volume, but baseline MTT sq lesions were significantly larger. The correlation with final T 2 WI lesion volume was strongest for DWI (Spearman rank correlation coefficient ρ=0.68), intermediate for CBF sq (ρ=0.55), and weakest for MTT sq (ρ=0.49) baseline lesion volumes. Neither DWI/CBF sq nor DWI/MTT sq mismatch predicted lesion growth; lesion growth was equally common in those with and without mismatch. Conclusions— Of the 2 PWI parameters, CBF sq lesions most closely identifies, and MTT sq overestimates, final T 2 WI lesion volume. “DWI/PWI mismatch” does not identify lesion growth. Patients without “DWI/PWI mismatch” are equally likely to have lesion growth as those with mismatch and should not be excluded from acute stroke treatment.

Background and Purpose— Choline and creatine are commonly used as denominators for other metabolites in ischemic stroke spectroscopy, assuming that they do not change. We investigated their concentration variation over time after stroke. Methods— Choline and creatine concentrations were measured by proton MR spectroscopic imaging in 51 patients at 5 times up to 3 months after stroke. Results— Choline and creatine levels changed significantly in the ischemic region. Choline was significantly reduced during the first 2 weeks after stroke onset ( P =0.034). Creatine was significantly reduced during the whole period of the study ( P =0.011). Conclusion— Choline and creatine concentrations are not reliable denominators for metabolite ratios in acute stroke because their levels vary significantly in ischemic brain regions.