Martina Absinta1, Irene C M Cortese2, Luisa Vuolo2, Govind Nair2, Manori P de Alwis2, Joan Ohayon2, Alessandro Meani2, Vittorio Martinelli2, Roberta Scotti2, Andrea Falini2, Bryan R Smith2, Avindra Nath2, Steven Jacobson2, Massimo Filippi2, Daniel S Reich1. 1. From the Division of Neuroimmunology and Neurovirology (M.A., I.C.M.C., L.V., G.N., M.P.d.A., J.O., B.R.S., A.N., S.J., D.S.R.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; and the Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience (M.A., A.M., M.F.), Department of Neurology (V.M.), and Department of Neuroradiology (R.S., A.F.), San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy. martina.absinta@nih.gov daniel.reich@nih.gov. 2. From the Division of Neuroimmunology and Neurovirology (M.A., I.C.M.C., L.V., G.N., M.P.d.A., J.O., B.R.S., A.N., S.J., D.S.R.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; and the Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience (M.A., A.M., M.F.), Department of Neurology (V.M.), and Department of Neuroradiology (R.S., A.F.), San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy.
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.
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.
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