The clinical relevance of correcting susceptibility-related distortions using a recently-developed dynamic distortion correction (DDC) approach is assessed. This was applied in fMRI data acquired from a group of 12 patients with a range of neuropathologies at 7 T. Despite the presence of pathologies, time series of artifact-free field maps were generated. If distortion correction was neglected, substantial displacements, both in EPI geometry and activation, were observed. Two cases with potential clinical implications were identified. The DDC was able to accurately correct distortions in all cases and is shown to be effective and clinically relevant in presurgical planning at 7 T.
Comparison of DDC and noDC EPI runs with reference GE images indicated that warps seen in noDC data were effectively removed by DDC in all patients. Figure 2 illustrates two cases in which susceptibility-related geometric distortion resulted in clinically relevant shifts in activation. In P3, a large region of susceptibility-related distortion was visible in M1 in the mean noDC EPI. Here, voxel shifts up to 5.1 mm (see “mean VSM”) were found. The std VSM showed relatively larger values (~1 mm) in the vicinity of the pathology for this patient. In P4, a shift in M1 of ~3.4 mm and low std VSM were observed. These shifts were corrected accurately by DDC as demonstrated by the good correspondence to the distortion-free GE reference. Smaller shifts of ~2 mm were present in four patients and to a negligible extent in the remaining four.
Shifts in activation of ~3.4 mm were observed in three patients, reaching over 5.1 mm in more lateral areas of M1 in P3 (Figure 3). These shifts were smaller (~1.7 mm) in five patients, and negligible in two. Two cases with clinically relevant shifts in activation were found (P3 and P4, Figure 3). In P3, activation may wrongly be judged to originate from the strong susceptibility-related artifact. With DDC, however, the activation perfectly overlays M1. In P4, with noDC, the most statistically significant activation appeared to be in the middle part of the precentral gyrus, hindering unique identification of the central sulcus. The activation could be interpreted as reflecting viable primary motor cortex. Following DDC, activation was shifted into the post-central gyrus, a correction which was established as being accurate (see P4, Figure 2). In this case, DDC is likely to change the clinician’s interpretation to suggest that, in fact, primary motor cortex is compromised and function has been reallocated to the post-central gyrus.
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