Is there an apparent diffusion coefficient threshold in predicting tissue viability in hyperacute stroke? (1/2665)

BACKGROUND AND PURPOSE: Rapid and precise identification of the penumbra is important for decision-making in acute stroke. We sought to determine whether an early and moderate decrease in the apparent diffusion coefficient (ADC) may help to identify, within the diffusion/perfusion (DWI/PWI) mismatch, those areas that will eventually evolve toward infarction. METHODS: We reviewed 48 patients not treated by thrombolytics who had a DWI/PWI within 6 hours after onset, with infarct evolution documented by follow-up magnetic resonance on days 2 to 4. We calculated absolute values for ADC and the ADC ratio (ADCr) in (1) the initial DWI hypersignal; (2) the final volume of the infarct, ie, the follow-up fluid-attenuated inversion recovery abnormalities; (3) the infarct growth (IGR) area; and (4) the oligemic area (OLI) that remained viable despite initial hemodynamic disturbance. We tested the value of the ADC to predict tissue outcome by using discriminant analysis. RESULTS: ADC values were marginally but significantly decreased in the IGR area (ADC 782+/-82x10(-6) mm(2)/s, ADCr 0.94+/-0.08) compared with mirror values (P=0.01) and with OLI (ADC 823+/-41x10(-6) mm(2)/s, ADCr 0.99+/-0.07; P=0.001). Of all quantitative DWI and PWI parameters, the ADCr best discriminated between IGR and OLI (F(1,50)=13.6, cutoff=0.97, 64% sensitivity, 92% specificity) and between the final volume of infarct and OLI (F(1,83)=219, cutoff=0.91, 91% sensitivity, 100% specificity). CONCLUSIONS: A simple approach based on ADC alone may allow the identification of tissue at risk of infarction in acute-stroke patients.  (+info)

DWI prediction of symptomatic hemorrhagic transformation in acute MCA infarct. (2/2665)

PURPOSE: Symptomatic hemorrhagic transformation is a severe complication of acute ischemic stroke which occurs at a higher frequency after thrombolysis. The present study was designed to analyze whether early DWI can be used for predicting the risk of hemorrhagic transformation with clinical worsening in MCA stroke patients. MATERIALS AND METHODS: Of 28 patients with a middle cerebral artery (MCA) infarct and proven MCA or carotid T occlusion on DWI and MR angiography performed within 14 hours after onset (mean 6.5 +/- 3.5 hours, median 5.2 hours), 4 developed hemorrhagic transformation with clinical worsening, while 24 did not. For the 2 groups, we compared admission NIHSS score, site of arterial occlusion, volume of DWI abnormalities, and several apparent diffusion coefficient (ADC) measurements: ADC(infarct) (mean ADC value of the whole infarct), ADC(core) (peak ADC decrease as calculated in a 57 mm(2) circular ROI, manually centered on the ischemic area with the lowest ADC value on the ADC maps), ADC(superficial) and ADC(deep). Discriminant function analysis was used to determine the most accurate predictors of symptomatic hemorrhagic transformation. RESULTS: The best predictor was the ADC(core) (F=5.34, p=2.9%, cut-off value=300 x 10(-6) mm(2)/s). This monovariate model allowed to correctly classify all 4 patients (ADC(core) 300 x 10(-6) mm(2)/s) with subsequent symptomatic hemorrhage, and 17 of the 24 patients without symptomatic hemmorrhage (ADC(core)>300 x 10(-6) mm(2)/s) (100% sensitivity, 71% specificity). CONCLUSION: Although preliminary, these results suggest that a simple measurement of minimum ADC values within an acute MCA stroke could be useful in targeting those patients with a high risk of severe hemorrhagic transformation.  (+info)

Diffusion-weighted imaging in a case of wernicke encephalopathy. (3/2665)

In a chronic alcoholic patient with progressive confusion, which was consistent with the clinical diagnosis of Wernicke encephalopathy, T2-weighted, FLAIR and diffusion weighted (DWI) MR imaging depicted brain abnormalities located in both medial thalamic nuclei. Apparent Diffusion Coefficient (ADC) measurements in these regions shown unexpected normal values, referring to Wernicke pathological findings and DWI data. DWI may be helpful to diagnose early basal nuclei abnormalities, but may fail to compute ADC values in these locations.  (+info)

Human brain hemorrhage: quantification of perihematoma edema by use of diffusion-weighted MR imaging. (4/2665)

BACKGROUND AND PURPOSE: Animal models have clearly shown a critical role for extravascular blood in the initiation of the vasogenic edema associated with intracerebral hemorrhage (ICH). Nevertheless, the relevance of these observations to the human disease process has not been evaluated. With a prospectively collected cohort of nine patients, we report the relation between intraparenchymal blood clot volume and elevation of perihematoma brain tissue (and homologous contralateral brain tissue) apparent diffusion coefficient (ADC). METHODS: Patients with acute and subacute supratentorial ICH were prospectively evaluated by using diffusion-weighted imaging. ADC was measured in perihematoma tissue and in homologous contralateral regions. The relationship between ADC and volume of hematoma was determined by using linear regression analysis. RESULTS: Nine patients were enrolled in the study. The mean hematoma volume was 30.8 cc (range, 2.6-74 cc). The ADC in the perihematoma regions was 172.5 x 10(-5) mm(2)/s (range, 120.1-302.5 x 10(-5) mm(2)/s) and in the contralateral corresponding regions of interest was 87.6 x 10(-5) mm(2)/s (range, 76.5-102.1 x 10(-5) mm(2)/s) (P=.02). The Pearson correlation coefficient for the ADC in surrounding edema and hematoma volume was 0.7 (P=.04). The correlation coefficient between hematoma volume and contralateral hemisphere ADC was 0.8 (P=.02). CONCLUSION: We report a significant direct correlation between ICH volume and degree of ADC elevation in perihematoma and ADC values in contralateral corresponding brain tissue. These findings suggest a dose-effect interaction between volume and concentration of blood products and intensity of response that brain tissue exhibits in blood-mediated edema. Prospective natural history and interventional studies are required to confirm this biologically meaningful correlation in patients with ICH.  (+info)

Metachromatic leukodystrophy: diffusion MR imaging findings. (5/2665)

Herein the case of a 10-month-old boy with metachromatic leukodystrophy is reported. Diffusion MR imaging performed with an echo-planar trace sequence revealed a cytotoxic edema-like pattern (high signal intensity on b = 1000 s/mm(2) images and low apparent diffusion coefficient values) in the affected white matter in the absence of an ischemic condition. This finding was unchanged at a 6-month follow-up, as revealed by diffusion MR imaging. A gradient-echo diffusion sequence, reverse fast imaging in steady-state precession, revealed hyperintense changes at the corresponding regions. It is likely that the cytotoxic edematous pattern (restricted diffusion pattern) reflected restriction of mobility of the water molecules within abnormal portions of the myelin sheath, because impaired myelin breakdown and reutilization are known features of metachromatic leukodystrophy.  (+info)

Cortical spreading depression in the feline brain following sustained and transient stimuli studied using diffusion-weighted imaging. (6/2665)

Cortical spreading depression (CSD) was induced by transient (10 min) applications of KCl in agar upon the cortical surface of alpha-chloralose anaesthetised cats. Its features were compared with CSD resulting from sustained applications of crystalline KCl through a mapping of the apparent diffusion coefficient (ADC) using diffusion-weighted echo planar imaging (DWI) over a poststimulus period of 60-100 min. Individual CSD events were computationally detected with the aid of Savitzky-Golay smoothing applied to critically sampled data derived from regions of interest (ROIs) made up of 2 x 2 pixel matrices. The latter were consistently placed at three selected sites on the suprasylvian gyrus (SG) and six sites on the marginal gyrus (MG). The CSD events thus detected were then quantitatively characterised for each ROI using the original time series. Both stimuli consistently elicited similar spreading patterns of initial, primary CSD events that propagated over the SG and marginal MG and were restricted to the hemispheres on which the stimuli were applied. There followed secondary events over smaller extents of cortical surface. Sustained stimuli elicited primary and secondary CSD events with similar amplitudes of ADC deflection that were distributed around a single mean. The ADC deflections were also conserved in peak amplitude throughout the course of their propagation. The initial primary event showed a poststimulus latency of 1.1 +/- 0.1 min. Successive secondary events followed at longer, but uniform, time intervals of around 10 min. Primary and secondary CSDs showed significantly different velocities of conduction (3.32 +/- 0.43 mm min(-1) vs. 2.11 +/- 0.21 mm min(-1), respectively; n = 5) across the cerebral hemisphere. In contrast, transient stimuli produced significantly fewer numbers of CSD events (3.8 +/- 0.5 events per animal, n = 5) than did sustained stimuli (7.4 +/- 0.5 events per animal, mean +/- S.E.M., n = 5, P = 0.002). The peak ADC deflection of their primary CSD events declined by approximately 30 % as they propagated from their initiation site to the interhemispheric boundary. The primary CSD event following a transient stimulus showed a latency of 1.4 +/- 0.1 min. It was followed by successive and smaller secondary ADC deflections that were separated by progressively longer time intervals. Conduction velocities of secondary events were similar to those of primary events. Conduction velocities of both primary and secondary events were slower than their counterparts following a sustained stimulus. ADC changes associated with CSD thus persist at times well after stimulus withdrawal and vary markedly with the nature of the initiating stimulus even in brain regions remote from the stimulus site.  (+info)

Diffusion-tensor MR imaging of gray and white matter development during normal human brain maturation. (7/2665)

BACKGROUND AND PURPOSE: Conventional MR imaging findings of human brain development are thought to result from decreasing water content, increasing macromolecular concentration, and myelination. We use diffusion-tensor MR imaging to test theoretical models that incorporate hypotheses regarding how these maturational processes influence water diffusion in developing gray and white matter. METHODS: Experimental data were derived from diffusion-tensor imaging of 167 participants, ages 31 gestational weeks to 11 postnatal years. An isotropic diffusion model was applied to the gray matter of the basal ganglia and thalamus. A model that assumes changes in the magnitude of diffusion while maintaining cylindrically symmetric anisotropy was applied to the white matter of the corpus callosum and internal capsule. Deviations of the diffusion tensor from the ideal model predictions, due to measurement noise, were estimated by using Monte Carlo simulations. RESULTS: Developing gray matter of the basal ganglia and developing white matter of the internal capsule and corpus callosum largely conformed to theory, with only small departures from model predictions in older children. However, data from the thalamus substantially diverged from predicted values, with progressively larger deviations from the model with increasing participant age. CONCLUSION: Changes in water diffusion during maturation of central gray and white matter structures can largely be explained by theoretical models incorporating simple assumptions regarding the influence of brain water content and myelination, although deviations from theory increase as the brain matures. Diffusion-tensor MR imaging is a powerful method for studying the process of brain development, with both scientific and clinical applications.  (+info)

Experimental cerebral fat embolism: embolic effects of triolein and oleic acid depicted by MR imaging and electron microscopy. (8/2665)

BACKGROUND AND PURPOSE: In fat embolism, free fatty acid is more toxic than neutral fat in terms of tissue damage. We evaluated the hyperacute embolic effects of triolein and oleic acid in cat brains by using MR imaging and electron microscopy. METHODS: T2-weighted imaging, diffusion-weighted imaging, and contrast-enhanced T1-weighted imaging were performed in cat brains after the injection of triolein (group 1, n = 8) or oleic acid (group 2, n = 10) into the internal carotid artery. MR images were quantitatively assessed by comparing the signal intensity ratios of the lesions with their counterparts on T2-weighted images, apparent diffusion coefficient (ADC) maps, and contrast-enhanced T1-weighted images. Electron microscopic findings in group 1 were compared with those in group 2. RESULTS: Qualitatively, MR images revealed two types of lesions. Type 1 lesions were hyperintense on diffusion-weighted images and hypointense on ADC maps. Type 2 lesions were isointense or mildly hyperintense on diffusion-weighted images and isointense on ADC maps. Quantitatively, the signal intensity ratios of type 1 lesions in group 2 specimens were significantly higher on T2-weighted images (P =.013)/(P =.027) and lower on ADC maps compared with those of group 1. Electron microscopy of type 1 lesions in both groups revealed more prominent widening of the perivascular space and swelling of the neural cells in group 2, in contrast to notable endothelial defects in group 1. CONCLUSION: MR and electron microscopic data on cerebral fat embolism induced by either triolein or oleic acid revealed characteristics suggestive of both vasogenic and cytotoxic edema in the hyperacute stage. Tissue damage appeared more severe in the oleic acid group than in the triolein group.  (+info)