Quantifying T2 relaxation time changes within lesions defined by apparent diffusion coefficient in grey and white matter in acute stroke patients

The apparent diffusion coefficient (ADC) of cerebral water, as measured by diffusion MRI, rapidly decreases in ischaemia, highlighting a lesion in acute stroke patients. The MRI T 2 relaxation time changes in ischaemic brain such that T 2 in ADC lesions may be informative of the extent of tissue damage, potentially aiding in stratification for treatment. We have developed a novel user-unbiased method of determining the changes in T 2 in ADC lesions as a function of clinical symptom duration based on voxel-wise referencing to a contralateral brain volume. The spherical reference method calculates the most probable pre-ischaemic T 2 on a voxel-wise basis, making use of features of the contralateral hemisphere presumed to be largely unaffected. We studied whether T 2 changes in the two main cerebral tissue types, i.e. in grey matter (GM) and white matter (WM), would differ in stroke. Thirty-eight acute stroke patients were accrued within 9 h of symptom onset and scanned at 3 T for 3D T 1-weighted, multi b-value diffusion and multi-echo spin echo MRI for tissue type segmentation, quantitative ADC and absolute T 2 images, respectively. T 2 changes measured by the spherical reference method were 1.94  ±  0.61, 1.50  ±  0.52 and 1.40  ±  0.54 ms h−1 in the whole, GM, and WM lesions, respectively. Thus, T 2 time courses were comparable between GM and WM independent of brain tissue type involved. We demonstrate that T 2 changes in ADC-delineated lesions can be quantified in the clinical setting in a user unbiased manner and that T 2 change correlated with symptom onset time, opening the possibility of using the approach as a tool to assess severity of tissue damage in the clinical setting

Quantitative chemical exchange saturation transfer imaging of nuclear overhauser effects in acute ischemic stroke

Purpose: In chemical exchange saturation transfer imaging, saturation effects between (Formula presented.) 2 to (Formula presented.) 5 ppm (nuclear Overhauser effects, NOEs) have been shown to exhibit contrast in preclinical stroke models. Our previous work on NOEs in human stroke used an analysis model that combined NOEs and semisolid MT; however their combination might feasibly have reduced sensitivity to changes in NOEs. The aim of this study was to explore the information a 4-pool Bloch–McConnell model provides about the NOE contribution in ischemic stroke, contrasting that with an intentionally approximate 3-pool model. Methods: MRI data from 12 patients presenting with ischemic stroke were retrospectively analyzed, as well as from six animals induced with an ischemic lesion. Two Bloch–McConnell models (4 pools, and a 3-pool approximation) were compared for their ability to distinguish pathological tissue in acute stroke. The association of NOEs with pH was also explored, using pH phantoms that mimic the intracellular environment of naïve mouse brain. Results: The 4-pool measure of NOEs exhibited a different association with tissue outcome compared to 3-pool approximation in the ischemic core and in tissue that underwent delayed infarction. In the ischemic core, the 4-pool measure was elevated in patient white matter ((Formula presented.)) and in animals ((Formula presented.)). In the naïve brain pH phantoms, significant positive correlation between the NOE and pH was observed. Conclusion: Associations of NOEs with tissue pathology were found using the 4-pool metric that were not observed using the 3-pool approximation. The 4-pool model more adequately captured in vivo changes in NOEs and revealed trends depending on tissue pathology in stroke

Lacunar Infarction Associated with Anabolic Steroids and Polycythemia: A Case Report

Lacunar infarction is traditionally ascribed to lipohyalinosis or microatheroma. We report the case of 40-year-old man, without traditional risk factors for ischemic stroke, who presented to the Emergency Department with recurrent episodes of transient right-sided weakness and paresthesia. Lacunar infarction was confirmed on diffusion-weighted MRI and blood tests showed a marked polycythemia. Quantitative magnetic resonance perfusion imaging demonstrated dramatically abnormal perfusion throughout both cerebral hemispheres, and transcranial Doppler revealed reduced cerebral artery velocities, both consistent with the proposed mechanism of hyperviscosity. His symptoms settled with treatment of the polycythemia and workup did not find another cause of ischemic stroke. We propose that hyperviscosity secondary to steroid-induced polycythemia caused ischemia in this case and not lipohyalinosis or microatheroma, to which lacunar disease is commonly attributed