Quantitative susceptibility mapping (QSM) has enabled MRI of tissue magnetic susceptibility to advance from simple qualitative detection of hypointense blooming artifacts to precise quantitative measurement of spatial biodistributions. QSM technology may be regarded to be sufficiently developed and validated to warrant wide dissemination for clinical applications of imaging isotropic susceptibility, which is dominated by metals in tissue, including iron and calcium. These biometals are highly regulated as vital participants in normal cellular biochemistry, and their dysregulations are manifested in a variety of pathologic processes. Therefore, QSM can be used to assess important tissue functions and disease. To facilitate QSM clinical translation, this review aims to organize pertinent information for implementing a robust automated QSM technique in routine MRI practice and to summarize available knowledge on diseases for which QSM can be used to improve patient care. In brief, QSM can be generated with postprocessing whenever gradient echo MRI is performed. QSM can be useful for diseases that involve neurodegeneration, inflammation, hemorrhage, abnormal oxygen consumption, substantial alterations in highly paramagnetic cellular iron, bone mineralization, or pathologic calcification; and for all disorders in which MRI diagnosis or surveillance requires contrast agent injection. Clinicians may consider integrating QSM into their routine imaging practices by including gradient echo sequences in all relevant MRI protocols.

This study demonstrates the dependence of non-local susceptibility effects on object orientation in gradient echo MRI and the reduction of non-local effects by deconvolution using quantitative susceptibility mapping (QSM). Imaging experiments were performed on a 3T MRI system using a spoiled 3D multi-echo GRE sequence on phantoms of known susceptibilities, and on human brains of healthy subjects and patients with intracerebral hemorrhages. Magnetic field measurements were determined from multiple echo phase data. To determine the QSM, these field measurements were deconvolved through a dipole inversion kernel under a constraint of consistency with the magnitude images. Phantom and human data demonstrated that the hypointense region in GRE magnitude image corresponding to a susceptibility source increased in volume with TE and varied with the source orientation. The induced magnetic field extended beyond the susceptibility source and varied with its orientation. In QSM, these blooming artifacts, including their dependence on object orientation, were reduced and material susceptibilities were quantified.

Purpose To investigate the magnetic susceptibility of intracerebral hemorrhages (ICH) at various stages by applying quantitative susceptibility mapping (QSM). Materials and Methods Blood susceptibility was measured serially using QSM after venous blood withdrawal from healthy subjects. Forty-two patients who provided written consent were recruited in this institutional review board approved study. Gradient echo MRI data of the 42 patients (17 females; 64±12 yrs) with ICH were processed with QSM. The susceptibilities of various blood products within hematomas were measured on QSM. Results Blood susceptibility continually increased and reached a plateau 96 hours after venous blood withdrawal. Hematomas at all stages were consistently hyperintense on QSM. Susceptibility was 0.57 ± 0.48, 1.30 ± 0.33, 1.14 ± 0.46, 0.40 ± 0.13, and 0.71 ± 0.31 parts per million (ppm) for hyperacute, acute, early subacute, late subacute and chronic stages of hematomas respectively. The susceptibility decrease from early subacute (1.14ppm) to late subacute (0.4ppm) was significant (p<0.01). Conclusion QSM reveals positive susceptibility in hyperacute hematomas, indicating that even at their hyperacute stage, deoxyhemoglobin may exist throughout the hematoma volume, not just at its rim as seen on conventional T2* imaging. QSM also reveals reduction of susceptibility from early subacute to late subacute ICH, suggesting that methemoglobin concentration decreases at the late subacute stage.