White Matter Hypointensities Research Articles

Axonal loss in multiple sclerosis lesions: Magnetic resonance imaging insights into substrates of disability

Magnetic resonance imaging (MRI) monitoring of disease progression in multiple sclerosis is limited by the lack of correlation of abnormalities seen on T2-weighted imaging, and disability. We studied the histopathology of multiple sclerosis lesions, as depicted by MRI, in a large postmortem sample, focusing on axonal loss. Tissue samples from 17 patients were selected immediately postmortem for histopathological analysis on the basis of T2-weighted imaging, including normal appearing white matter and T1 hypointense lesions. In each region, we measured magnetization transfer ratios (MTR), T1 contrast ratio, myelin, and axonal density. T2 lesions (109 samples) were heterogeneous with regard to MRI appearance on T1 and MTR, whereas axonal density ranged from 0% (no residual axons) to 100% (normal axonal density). Of 64 T2 lesions, 17 were reactive (mild perivascular inflammation only), 21 active, 15 chronically active, and 11 chronically inactive. MTR and T1 contrast ratio correlated strongly with axonal density. Also in normal appearing white matter (24 samples), MTR correlated with axonal density. In conclusion, postmortem tissue sampling by using MRI revealed a range of pathology, illustrating the high sensitivity and low specificity of T2-weighted imaging. T1 hypointensity and MTR were strongly associated with axonal density, emphasizing their role in monitoring progression in multiple sclerosis.

MR imaging of hemorrhagic conditions of the head and neck.

1. There is a constant sequence of signal intensity patterns that characterize 1.5 T, spin echo MR images of hemorrhagic lesions. 2. The MRI appearance of intraparenchymal hemorrhage is determined by the sequential chemical degradation of Hb, by the paramagnetic properties of the degradation products and by certain biologic factors including pO2, edema formation, hematocrit and BBB. 3. Acute intraparenchymal hemorrhage is characterized by markedly diminished signal intensity centrally relative to surrounding white matter (hypointensity) on T2 weighted images and often by a moderately increased signal intensity (hyperintensity) of the adjacent white matter produced by surrounding edema on proton density and T2 weighted images. 4. Early subacute intraparenchymal hemorrhage is characterized centrally by moderate hypointensity on T2 weighted images, and peripherally, by moderate hyperintensity on T1 weighted and marked hypointensity on T2 weighted images. Hyperintensity on proton density and T2 weighted images of nearby white matter owing to edema may again be seen. 5. Late subacute intraparenchymal hemorrhage is characterized by marked peripheral and central hyperintensity on both T1 and T2 weighted images. Also, marked hypointensity of the adjacent brain rim on T2 weighted images owing to hemosiderin deposition may be seen. 6. Chronic intraparenchymal hemorrhage is characterized by marked hyperintensity both centrally and peripherally on both T1 and T2 weighted images and by marked hypointensity of the adjacent brain rim on T2 weighted images owing to hemosiderin deposition. Surrounding edema is no longer present. 7. The integrity of the blood-brain barrier appears to be important in determining whether or not hemosiderin accumulations consistently occur in subacute and chronic hemorrhage. 8. Hemorrhagic conditions in which the defined sequence of signal intensity patterns may be seen include: venous thrombosis, hemorrhagic infarction, occult vascular malformation and intracranial aneurysm.

Errors in Regard to Goitre

ABSTRACT Background Regional changes to cortical thickness in individuals with neurodegenerative and cerebrovascular diseases can be estimated using specialised neuroimaging software. However, the presence of cerebral small vessel disease, focal atrophy, and cortico-subcortical stroke lesions, pose significant challenges that increase the likelihood of misclassification errors and segmentation failures. Purpose The main goal of this study was to examine a correction procedure developed for enhancing FreeSurfer’s cortical thickness estimation tool, particularly when applied to the most challenging MRI obtained from participants with chronic stroke and cerebrovascular disease, with varying degrees of neuro-vascular lesions and brain atrophy. Methods In 155 cerebrovascular disease patients enrolled in the Ontario Neurodegenerative Disease Research Initiative (ONDRI), FreeSurfer outputs were compared between a fully automated, unmodified procedure and a corrected procedure that accounted for potential sources of error due to atrophy and neurovascular lesions. Quality control (QC) measures were obtained from both procedures. Association between cortical thickness and global cognitive status as assessed by the Montreal Cognitive Assessment (MoCA) score was also investigated from both procedures. Results Corrected procedures increased ‘Acceptable’ QC ratings from 18% to 76% for the cortical ribbon and from 38% to 92% for tissue segmentation. Corrected procedures reduced ‘Fail’ ratings from 11% to 0% for the cortical ribbon and 62% to 8% for tissue segmentation. FreeSurfer-based segmentation of T1-weighted white matter hypointensities were significantly greater in the corrected procedure (5.8mL vs. 15.9mL, p Conclusions These findings suggest that correction procedures that account for brain atrophy and neurovascular lesions can significantly improve FreeSurfer’s segmentation results, reduce failure rates, and potentially increase sensitivity to examine brain-behaviour relationships. Future work will examine relationships between cortical thickness, cerebral small vessel disease, and neurodegenerative disease in the ONDRI study.