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Optimizing brain MRI protocols in the follow-up of patients with multiple sclerosis: T2-weighted MRI of the brain after the administration of gadopentetate dimeglumine

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Zitation

Taschner, C., Kirsch, E., Scheffler, K., Wetzel, S., Schulte-Mönting, J., Kappos, L., et al. (2005). Optimizing brain MRI protocols in the follow-up of patients with multiple sclerosis: T2-weighted MRI of the brain after the administration of gadopentetate dimeglumine. Magnetic Resonance Imaging, 23(3), 469-474. doi:10.1016/j.mri.2004.12.007.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-0013-D5CB-5
Zusammenfassung
The aim of our study was to determine whether T2-weighted (T2w) MRI of the brain could be performed immediately after the administration of gadopentetate dimeglumine (gadolinium DTPA) in patients with multiple sclerosis (MS) without a loss in image quality or diagnostic reliability. Sixteen patients with clinically diagnosed MS were included in the study. Twenty-four patients with various cerebral pathologies (14 patients with multiple lacunar lesions) were examined in order to exclude masking of T2 hyperintense lesions other than MS lesions. Images of 10 patients without pathological changes served as a control condition for the qualitative analysis. In these 50 patients, T1w and T2w MRI was performed before and after the administration of gadolinium DTPA. Signal intensities were measured within T2 hyperintense cerebral lesions, in T1-enhancing lesions and in normal appearing brain tissue on T2w turbo spin-echo (TSE) sequences. Both quantitative and qualitative analysis did not show significant differences between T2w pre- and postcontrast series. T2w MRI performed prior to and after the administration of gadolinium DTPA provides similar information in patients with MS. With a TR of 3.2 s, not a single lesion was obscured on T2w postcontrast series.
Acquisition of T2w MR images immediately after the administration of gadolinium DTPA allows for shorter examination time and assures sufficient time for contrast enhancement in cerebral lesions with a disrupted blood–brain barrier.