Evolution of acute "black hole" lesions in patients with relapsing-remitting multiple sclerosis
- PMID: 35397094
- DOI: 10.1007/s13760-022-01938-9
Evolution of acute "black hole" lesions in patients with relapsing-remitting multiple sclerosis
Abstract
Objective: Gadolinium-enhanced T1-weighted lesions are a well-established marker of areas with acute inflammatory activity. A majority of these gadolinium-enhanced T1 lesions are isointense relative to the surrounding white matter, but 20-40% of such active lesions will evolve during one year into areas of low signal ("black hole"). This study sought to characterize evolution of "black hole" lesions in patients with relapsing-remitting multiple sclerosis (MS) using the magnetic resonance imaging (MRI), which measures active lesions via the count of new or enlarged T2 and gadolinium-enhanced T1-weighted lesions.
Materials and methods: This was a prospective, observational case-series study which utilized pre- and post-gadolinium contrast T1-weighted and Proton density MRI scans. Twenty-nine patients (8 males and 21 females) with average age of 38.86 ± 6.58 years and disease duration of 5.75 ± 7.00 years were used to analyze 196 acute demyelinating plaques detected on MRI images during the 24-month follow-up of post-gadolinium signal intensity enhancement of MS plaques.
Results: Significant difference in black hole development was found between the shapes of acute and chronic "black holes". Ring-shaped and patchy plaques were 4.09 (1.87-8.91) times more likely and 1.49 (0.71-3.12) times less likely to develop an acute "black holes" than homogeneous plaques, respectively. Acute plaques with higher lesion-to-CSF SI ratio and larger surface area showed a greater tendency to develop into acute and chronic "black holes".
Conclusions: The value of lesion-to-CSF SI ratio and surface area were found as the predictors of the "black hole" formation.
Keywords: 3 T magnet; Acute black holes; Magnetic resonance imaging; Multiple sclerosis; Proton density; T1-weighted.
© 2022. The Author(s) under exclusive licence to Belgian Neurological Society.
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