Leptomeningeal gadolinium enhancement across the spectrum of chronic neuroinflammatory diseases

Martina Absinta, Irene C.M. Cortese, Luisa Vuolo, Govind Nair, Manori P. De Alwis, Joan Ohayon, Alessandro Meani, Vittorio Martinelli, Roberta Scotti, Andrea Falini, Bryan R. Smith, Avindra Nath, Steven Jacobson, Massimo Filippi, Daniel S. Reich

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1439-1444
Number of pages6
JournalNeurology
Volume88
Issue number15
DOIs
StatePublished - Apr 11 2017

ASJC Scopus subject areas

  • Clinical Neurology

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