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000141398 1001_ $$aKarimian-Jazi, Kianush$$b0
000141398 245__ $$aGd contrast administration is dispensable in patients with MS without new T2 lesions on follow-up MRI.
000141398 260__ $$aPhiladelphia, Pa.$$bLippincott Williams & Wilkins$$c2018
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000141398 500__ $$aNeurology Neuroimmunology & Neuroinflammation
000141398 520__ $$aTo assess the diagnostic value of gadolinium (Gd) contrast administration in MRI follow-up examinations of patients with MS if the T2 lesion load is stable.We included 100 patients with MS with at least 2 cranial MRI follow-up examinations (mean follow-up time 4.0 ± 2.6 years). MRI was performed at 3 Tesla with a standardized protocol including T2-weighted, fluid-attenuated inversion recovery (FLAIR) and T1-weighted contrast-enhanced sequences. Images were analyzed for T2/FLAIR and contrast-enhancing (CE) lesions by 3 independent neuroradiologists. Isolated Gd-enhancing lesions without correlate in T2 and FLAIR images, and reactivated Gd+ lesions were further assessed for size and signal intensity.We identified a total of 343 new T2 lesions and 152 CE lesions in a total of 559 MRI follow-up examinations. New T2/FLAIR lesions were present in 30% of the scans. Of the Gd-enhancing lesions, 145/152 (95.4%) showed a correlate as a new T2/FLAIR lesion. There were 3 enhancing lesions (1.9% of all enhancing lesions) without T2/FLAIR correlate and 4 lesions (2.6%) that exhibited lesion reactivation or persistent enhancement over time. As a predictive factor of enhancement, we found that enhancing lesions had a higher T2 signal ratio (T2 SRlesion/normal-appearing white matter: 3.0 ± 0.1 vs 2.2 ± 0.1, p < 0.001).The likelihood of missing 'active lesions' is overall small (1.7%) if T2 lesions are stable compared with the previous MRI examination. Lesion reactivation is rare. Our study indicates that Gd contrast administration might be dispensable in follow-up MRI of patients with MS if no new T2/FLAIR lesions and no new neurologic symptoms are present.
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000141398 7001_ $$aWildemann, Brigitte$$b1
000141398 7001_ $$0P:(DE-He78)0b1c40947becd495c5aa9778ef098ef4$$aDiem, Ricarda$$b2$$udkfz
000141398 7001_ $$0P:(DE-He78)a46ef05266eafb5f42c207880f97ebf6$$aSchwarz, Daniel$$b3$$udkfz
000141398 7001_ $$0P:(DE-He78)743a4a82daab55306a2c88b9f6bf8c2f$$aHielscher, Thomas$$b4
000141398 7001_ $$0P:(DE-He78)92e9783ca7025f36ce14e12cd348d2ee$$aWick, Wolfgang$$b5
000141398 7001_ $$aBendszus, Martin$$b6
000141398 7001_ $$0P:(DE-He78)5ba5b48bd126214d9cb66291fa4ae303$$aBreckwoldt, Michael$$b7$$eLast author$$udkfz
000141398 773__ $$0PERI:(DE-600)2767740-0$$a10.1212/NXI.0000000000000480$$gVol. 5, no. 5, p. e480 -$$n5$$pe480$$tNeurology$$v5$$x2332-7812$$y2018
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