{'fraction_non_alphanumeric': 0.027168234064785787, 'fraction_numerical': 0.011494252873563218, 'mean_word_length': 6.044117647058823, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Controversial association between leptomeningeal enhancement and demyelinated cortical lesions in multiple sclerosis

Leptomeningeal enhancement (LME) is a novel imaging finding1 that has been detected on delayed postcontrast fluid-attenuated inversion recovery (FLAIR) images on high-field and ultra-high-field magnetic resonance imaging (MRI).1–5 LME has been postulated to be pathologically related to the disruption of the blood–meningeal barrier due to leptomeningeal inflammation1 and potentially ectopic B-cell folliclelike aggregations. In prior imaging studies, LME has been consistently implicated in cortical damage and thinning.1–5 There is substantial variability in the reported prevalence of LME,1–5 but one consistent finding is a greater frequency in progressive forms of multiple sclerosis (MS).1–3 There is also evidence that LME is not specific to MS occurring frequently in other inflammatory/infectious neurological disorders as well.6