Background. Brain lesions are common in neuromyelitis optica spectrum disorder (NMOsd) and may resemble lesions of multiple sclerosis (MS). Objectives. To describe the imaging characteristics of supratentorial lesions in NMOsd on ultrahigh-field (7？T) MRI with special attention to vessel-lesion relationship. Methods. Ten NMOsd patients, all women and all seropositive for NMO IgG, with mean age of 51.3 ± 15.4 years and disease duration of 9.2 ± 6.4 years, were scanned at a 7？T whole-body human MR system with high-resolution 2D gradient echo sequence optimized to best visualize lesions and venous structures, T2- and T1-weighted imaging. Results. In 10 patients with NMOsd, a total of 92 lesions were observed (mean: 9.2 ± 8.8; range: 2–30), but only 8 lesions (9%) were traversed by a central venule. All lesions were <5？mm in diameter, and 83% were located in subcortical white matter. There were no lesions in the cortex or basal ganglia. Two patients exhibited diffuse periependymal abnormalities on FLAIR. Conclusions. Small, subcortical lesions without a central venule are the most consistent finding of NMOsd on 7？T MRI of the brain. Ultrahigh-field imaging may be useful for differentiating between NMOsd and MS. 1. Introduction Neuromyelitis optica (NMO) has been traditionally considered a predominantly opticospinal disorder, but recent studies have shown that clinical spectrum of NMO includes cerebral and brainstem syndromes as well [1–3]. Brain lesions on magnetic resonance imaging (MRI) are found in the majority of NMO patients with long-standing disease [1, 2, 4–6], which makes it sometimes difficult to differentiate this disorder from multiple sclerosis (MS). Ultrahigh-field MRI (4 Tesla or above) affords an unprecedented view of brain structures and pathology in vivo on a submillimeter scale due to high signal-to-noise ratio [7, 8]. The largely enhanced susceptibility of ultrahigh-field MR effect provides unique contrast between lesions and veins. This feature makes ultrahigh-field MR a valuable tool for differentiating plaques of MS, which frequently contain a venule, from lesions of other etiologies that rarely do [9]. Our aim in this work is to characterize brain lesions in patients with neuromyelitis optica spectrum disorders (NMOsd) using 7？T MR and to discuss the findings in the context of the growing literature on ultrahigh-field imaging in MS [9–19]. 2. Methods Inclusion criteria in the study were the diagnosis of NMO-spectrum disorders (NMOsd) defined either as NMO by 2006 Wingerchuk et al. criteria [20], or recurrent longitudinally extensive
References
[1]
S. Jarius, K. Ruprecht, B. Wildemann, T. Kuempfel, M. Ringelstein, C. Geis, et al., “Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: a multicentre study of 175 patients,” Journal of Neuroinflammation, vol. 9, article 14, 2012.
[2]
S. H. Kim, W. Kim, X. F. Li, I. J. Jung, and H. J. Kim, “Clinical spectrum of CNS aquaporin-4 autoimmunity,” Neurology, vol. 78, no. 15, pp. 1179–1185, 2012.
[3]
B. F. G. Popescu, V. A. Lennon, J. E. Parisi et al., “Neuromyelitis optica unique area postrema lesions: nausea, vomiting, and pathogenic implications,” Neurology, vol. 76, no. 14, pp. 1229–1237, 2011.
[4]
S. J. Pittock, V. A. Lennon, K. Krecke, D. M. Wingerchuk, C. F. Lucchinetti, and B. G. Weinshenker, “Brain abnormalities in neuromyelitis optica,” Archives of Neurology, vol. 63, no. 3, pp. 390–396, 2006.
[5]
J. A. Cabrera-Gomez and I. Kister, “Conventional brain MRI in neuromyelitis optica,” European Journal of Neurology, vol. 19, no. 6, pp. 812–819, 2012.
[6]
S. H. Kim, S. Y. Huh, and H. J. Kim, “Brain abnormalities in neuromyelitis optica spectrum disorder,” Multiple Sclerosis International, vol. 2012, Article ID 735486, 10 pages, 2012.
[7]
A. G. van der Kolk, J. Hendrikse, and P. R. Luijten, “Ultrahigh-field magnetic resonance imaging: the clinical potential for anatomy, pathogenesis, diagnosis, and treatment planning in brain disease,” Neuroimaging Clinics of North America, vol. 22, no. 2, pp. 343–362, 2012.
[8]
I. D. Kilsdonk, W. L. de Graaf, F. Barkhof, and M. P. Wattjes, “Inflammation high-field magnetic resonance imaging,” Neuroimaging Clinics of North America, vol. 22, no. 2, pp. 135–157, 2012.
[9]
E. C. Tallantyre, J. E. Dixon, I. Donaldson et al., “Ultra-high-field imaging distinguishes MS lesions from asymptomatic white matter lesions,” Neurology, vol. 76, no. 6, pp. 534–539, 2011.
[10]
K. Kollia, S. Maderwald, N. Putzki et al., “First clinical study on ultra-high-field MR imaging in patients with multiple sclerosis: comparison of 1.5T and 7T,” American Journal of Neuroradiology, vol. 30, no. 4, pp. 699–702, 2009.
[11]
N. Mistry, E. C. Tallantyre, J. E. Dixon, et al., “Focal multiple sclerosis lesions abound in ‘ normal appearing white matter’,” Multiple Sclerosis, vol. 17, no. 11, pp. 1313–1323, 2011.
[12]
A. Kangarlu, E. C. Bourekas, A. Ray-Chaudhury, and K. W. Rammohan, “Cerebral cortical lesions in multiple sclerosis detected by MR imaging at 8 tesla,” American Journal of Neuroradiology, vol. 28, no. 2, pp. 262–266, 2007.
[13]
C. Mainero, T. Benner, A. Radding et al., “In vivo imaging of cortical pathology in multiple sclerosis using ultra-high field MRI,” Neurology, vol. 73, no. 12, pp. 941–948, 2009.
[14]
K. Schmierer, H. G. Parkes, P. W. So et al., “High field (9.4 Tesla) magnetic resonance imaging of cortical grey matter lesions in multiple sclerosis,” Brain, vol. 133, no. 3, pp. 858–867, 2010.
[15]
Y. Ge, V. M. Zohrabian, and R. I. Grossman, “Seven-tesla magnetic resonance imaging: new vision of microvascular abnormalities in multiple sclerosis,” Archives of Neurology, vol. 65, no. 6, pp. 812–816, 2008.
[16]
K. E. Hammond, M. Metcalf, L. Carvajal et al., “Quantitative in vivo magnetic resonance imaging of multiple sclerosis at 7 Tesla with sensitivity to iron,” Annals of Neurology, vol. 64, no. 6, pp. 707–713, 2008.
[17]
D. Pitt, A. Boster, W. Pei et al., “Imaging cortical lesions in multiple sclerosis with ultra-high-field magnetic resonance imaging,” Archives of Neurology, vol. 67, no. 7, pp. 812–818, 2010.
[18]
E. C. Tallantyre, M. J. Brookes, J. E. Dixon, P. S. Morgan, N. Evangelou, and P. G. Morris, “Demonstrating the perivascular distribution of ms lesions in vivo with 7-tesla MRI,” Neurology, vol. 70, no. 22, pp. 2076–2078, 2008.
[19]
T. Sinnecker, P. Mittelstaedt, J. D？rr et al., “Multiple sclerosis lesions and irreversible brain tissue damage: a comparative ultrahigh-field strength magnetic resonance imaging study,” Archives of Neurology, vol. 69, no. 6, pp. 739–745, 2012.
[20]
D. M. Wingerchuk, V. A. Lennon, S. J. Pittock, C. F. Lucchinetti, and B. G. Weinshenker, “Revised diagnostic criteria for neuromyelitis optica,” Neurology, vol. 66, no. 10, pp. 1485–1489, 2006.
[21]
P. J. Waters, A. McKeon, M. I. Leite, et al., “Serologic diagnosis of NMO: a multicenter comparison of aquaporin-4-IgG assays,” Neurology, vol. 78, no. 9, pp. 665–671, 2012.
[22]
E. Matsusue, S. Sugihara, S. Fujii, E. Ohama, T. Kinoshita, and T. Ogawa, “White matter changes in elderly people: MR-pathologic correlations,” Magnetic Resonance in Medical Sciences, vol. 5, no. 2, pp. 99–104, 2006.
[23]
A. L. Horowitz, R. D. Kaplan, G. Grewe, R. T. White, and L. M. Salberg, “The ovoid lesion: a new MR observation in patients with multiple sclerosis,” American Journal of Neuroradiology, vol. 10, no. 2, pp. 303–305, 1989.
[24]
F. Fazekas, R. Kleinert, H. Olfenbacher et al., “Pathologic correlates of incidental MRI white matter signal hyperintensities,” Neurology, vol. 43, no. 9, pp. 1683–1689, 1993.
[25]
P. Banker, S. Sonni, I. Kister, J. P. Loh, and Y. W. Lui, “Pencil-thin ependymal enhancement in neuromyelitis optica spectrum disorders,” Multiple Sclerosis, vol. 18, no. 7, pp. 1050–1053, 2012.
[26]
T. Makino, S. Ito, M. Mori, T. Yonezu, Y. Ogawa, and S. Kuwabara, “Diffuse and heterogeneous T2-hyperintense lesions in the splenium are characteristic of neuromyelitis optica,” Multiple Sclerosis. In press.
[27]
M. Calabrese, M. S. Oh, A. Favaretto, et al., “No MRI evidence of cortical lesions in neuromyelitis optica,” Neurology, vol. 79, no. 16, pp. 1671–1676, 2012.
[28]
T. Sinnecker, J. D？rr, C. F. Pfueller, L. Harms, K. Ruprecht, S. Jarius, et al., “Distinct lesion morphology at 7-T MRI differentiates neuromyelitis optica from multiple sclerosis,” Neurology, vol. 79, pp. 708–714, 2012.
[29]
B. F. G. Popescu, J. E. Parisi, J. A. Cabrera-Gómez, et al., “Absence of cortical demyelination in neuromyelitis optica,” Neurology, vol. 75, no. 23, pp. 2103–2109, 2010.
[30]
O. Ciccarelli, “Do cortical lesions help us to distinguish MS from NMO?” Neurology, vol. 79, no. 16, pp. 1630–1631, 2012.
[31]
N. Lummel, T. Boeckh-Behrens, V. Schoepf, M. Burke, H. Brückmann, and J. Linn, “Presence of a central vein within white matter lesions on susceptibility weighted imaging: a specific finding for multiple sclerosis?” Neuroradiology, vol. 53, no. 5, pp. 311–317, 2011.
[32]
V. G. Young, G. M. Halliday, and J. J. Kril, “Neuropathologic correlates of white matter hyperintensities,” Neurology, vol. 71, no. 11, pp. 804–811, 2008.
[33]
J. W. Dawson, “The histology of disseminated sclerosis,” Transactions of the Royal Society of Edinburgh, vol. 50, article 117, 1916.
