Leptomeningeal gadolinium enhancement across the spectrum of chronic neuroinflammatory diseases

M Absinta, ICM Cortese, L Vuolo, G Nair, MP De Alwis, J Ohayon, Alessandro Meani, V Martinelli, Raffaella Scotti, A Falini, BR Smith, A Nath, S Jacobson, M Filippi, DS Reich

Research output: Contribution to journalArticlepeer-review


Objective: To assess the prevalence and the specificity of leptomeningeal enhancement (LME) on postcontrast T2-fluid-attenuated inversion recovery (FLAIR) MRI in multiple sclerosis (MS) compared to a variety of inflammatory and noninflammatory neurologic conditions assessed in 2 academic research hospitals. Methods: On 3T postcontrast T2-FLAIR images, the presence of focal gadolinium enhancement was evaluated in the leptomeningeal compartment in 254 people with non-MS neurologic conditions or neurotropic viral infections. Based on their clinical diagnosis, patients were grouped as follows: (1) other-than-MS inflammatory neurologic diseases; (2) noninflammatory neurologic diseases; (3) human T-lymphotropic virus (HTLV)-infected; (4) HIV-infected; (5) healthy volunteers. Results: LME was detected in 56/254 non-MS cases (22%) vs 74/299 (25%) of MS cases. LME was nearly 4-fold more frequent in non-MS inflammatory neurologic conditions (18/51 cases, 35%) than in noninflammatory neurologic conditions (3/38, 8%) and healthy volunteers (5/66, 8%). The highest prevalence of LME was detected in HTLV infection (17/38 cases, 45%), particularly in the setting of HTLV-associated myelopathy (14/25 cases, 56%). LME also frequently occurred in HIV infection (13/61 cases, 21%). Unlike in MS, LME is not associated with lower brain and cortical volumes in non-MS inflammatory neurologic conditions, including HTLV and HIV infection. Conclusions: Despite its relevance to MS pathogenesis and cortical pathology, LME is not specific to MS, occurring frequently in non-MS inflammatory neurologic conditions and especially in those patients with HTLV-associated myelopathy. Overall, this strengthens the notion that LME localizes inflammation-related focal disruption of the blood-meninges barrier and associated scarring. © 2017 American Academy of Neurology.
Original languageEnglish
Pages (from-to)1439-1444
Number of pages6
Issue number15
Publication statusPublished - 2017


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