Leptomeningeal gadolinium enhancement across the spectrum of chronic neuroinflammatory diseases.

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.

Multiple sclerosis shrinks intralesional, and enlarges extralesional, brain parenchymal veins.

OBJECTIVES: Many multiple sclerosis (MS) lesions develop around small veins that are surrounded by perivenular inflammatory cells, but whether veins in the brains of people with MS are smaller or larger than similar veins in healthy volunteers or people with other neurologic diseases remains unknown. This question can be addressed by high-resolution, high-field-strength MRI. METHODS: In a cross-sectional study performed on a standard 3 T clinical scanner, we acquired whole-brain T2*-weighted images with 0.55 mm isotropic voxels and reconstructed the courses of deep and superficial veins within the white matter. We compared the apparent diameters of intralesional and perilesional veins to those of extralesional MS veins, veins in healthy volunteers, and veins in individuals with other neurologic diseases. RESULTS: We studied veins in 19 MS cases, 9 healthy volunteers, and 8 individuals with other neurologic diseases, analyzing a total of 349 veins. The mean diameter of intralesional veins (0.76 ± 0.14 mm) was smaller than that of perilesional (1.18 ± 0.13 mm; p < 0.001) and extralesional (1.13 ± 0.14 mm; p < 0.001) veins, regardless of lesion size and location. Perilesional and extralesional MS veins were larger than non-MS veins (0.94 ± 0.14 mm; p < 0.001), and intralesional MS veins were smaller (p < 0.001). CONCLUSIONS: The small apparent size of intralesional MS veins may reflect compression by the perivascular inflammatory cuff within active lesions or hardening of the vascular wall in chronic lesions. The finding that extralesional veins are larger than similar veins in non-MS lesions may result from diffuse disease-related processes.