Detecting lesions in multiple sclerosis at 4.7 tesla using phase susceptibility‐weighting and T2‐weighting

Abstract

Purpose: To demonstrate 4.7 Tesla (T) imaging methods for visualizing lesions in multiple sclerosis in the human brain using phase susceptibility-weighting and T2 weighting. Materials and Methods:Seven patients with relapsingremitting multiple sclerosis were imaged at 4.7T using three-dimensional (3D) susceptibility-weighted imaging (SWI) with 0.90 mm 3 voxel volumes, and with 2D T2-weighted fast spin echo (T2WFSE) with 0.34 mm 3 voxels and 1.84 mm 3 voxels. The visibility of MS lesions at 4.7T with phase SWI and T2WFSE was assessed by independent lesion counts made by an experienced neuroradiologist, and by quantitative measures. Results:High resolution T2WFSE at 4.7T provided excellent depiction of hyperintense lesions. When combined with phase SWI, 124 total lesions were identified of which 18% were only visible on phase SWI and not on T2WFSE. The phase lesions had a mean phase shift relative to local background of Ϫ11.15 Ϯ 5.97 parts per billion. Conclusion:Imaging at 4.7T can provide both high quality, high resolution T2WFSE and SWI for visualization of lesions in multiple sclerosis. Phase susceptibility-weighting can identify additional lesions that are not visible with high resolution T2WFSE.

Iron Deposition on SWI-Filtered Phase in the Subcortical Deep Gray Matter of Patients with Clinically Isolated Syndrome May Precede Structure-Specific Atrophy

“…1 GM damage is most extensive in patients with progressive MS, 2 but is already present in those with CIS [3][4][5][6][7][8][9][10] and can predict conversion to clinically definite MS. [11][12][13] Most authors investigating iron deposition in MS have used imaging techniques such as T2 hypointensity, [14][15][16] relaxometry, [17][18][19] magnetic field correlation, 20 and SWI. [21][22][23] Accumulation of iron in the SDGM has also been observed histologically in MS, 24,25 and iron deposition has been detected in the same SDGM structures where the volume loss also occurred. 23 It is thought that excessive levels of iron in the brain may lead to tissue damage by the generation of reactive oxygen species, most probably through the Fenton reaction.…”

“…24,25 More recently, MR imaging techniques, such as T2 relaxometry, [17][18][19] T2 hypointensity, [14][15][16]30,39 magnetic field correlation, 20 and SWI [21][22][23]40 have been used to quantify and visualize iron deposition in vivo. Looking at changes in T2 intensity is a relatively straightforward method of evaluating iron content, because increased levels of iron result in reduced T2 relaxation time, leading to hypointensity on T2-weighted images.…”

Assessing Abnormal Iron Content in the Deep Gray Matter of Patients with Multiple Sclerosis versus Healthy Controls

“…[7][8][9] Currently, there is an increased interest in studying how GM is affected 6,10,11 and particularly deep GM involvement in MS when iron deposition has been observed. 6,12,13 Brain iron accumulation in neurodegenerative diseases, including MS, is not new and has been shown histologically in the past. 14,15 In MS, its source is likely due to myelin or oligodendrocyte debris, concentrated iron in the macrophages, or as a product of local microhemorrhages following venule wall damage.…”

Phase White Matter Signal Abnormalities in Patients with Clinically Isolated Syndrome and Other Neurologic Disorders

“…17,32 Inversely, 12% of T2 WM-SAs overlapped with phase WM-SAs, a number in line with but slightly lower than that previously observed (16%-18%) at higher field strengths and in patients at a more advanced disease stage. 24,33 Even though this study demonstrates that the presence of phase WM-SAs is both sensitive (70.8%) and specific (76.6%) in distinguishing CIS and HCs, the benefit is not substantial compared with T2 WM-SAs. However, the presence of phase WMSAs had a high sensitivity and specificity in differentiating patients with CIS and OND, an observation that was even extended to differentiating patients with CIS from those with OND with autoimmune origin.…”