Document Type: Original Research


1 Department of Radiology, BSc of Radiology, School of Paramedical Sciences, Kurdistan University of Medical Sciences, Sanandaj, Iran

2 Department of Radiology, Faculty of Paramedical Sciences, Kurdistan University of Medical Sciences, Sanandaj, Iran

3 Professor Assistant of Radiology, Kurdistan Department of Radiology, Faculty of Medical Sciences, Kurdistan University of Medical Sciences, Sanandaj, Iran

4 MSc of Anatomy, Shahid Chamran MRI center, Kurdistan University of Medical Sciences, Sanandaj, Iran


Background: Multiple sclerosis (MS) is a chronic, typically progressive and most common autoimmune disease which damaged the central nervous system. According to the reports in 2008, this disorder has affected 2 and 2.5 million people globally. While the reason is not clear, proposed causes for this include immunologic, environmental, infectious and genetic factors, and sexuality. MS can cause many symptoms, including blurred vision, loss of balance, poor coordination, slurred speech, tremors, numbness, extreme fatigue, problems with memory and concentration, paralysis, blindness, and more. There are four distinguished illness fields in MS: relapsing-remitting MS (RRMS), primary-progressive MS (PPMS), secondary-progressive MS (SPMS), and progressive-relapsing. MRI is a great tool to identify the asymptomatic distribution of lesions in space and time.
Materials and Methods: 32 patients with MS plaques were evaluated by FLAIR and DWI pre- and post-Gadolinium injection compared with 15minutes delay T1w SE.
Results: FLAIR post-inject had significantly better detection of the number and signal intensity of active MS lesions. DWI and ADC images detected active plaques different from non-active lesions without contrast.
Conclusion: The result of this study showed that FLAIR post-inject had the highest sensitivity in detection of active MS lesions due to the CSF signal suppression in FLAIR, thus offering enough TR time recovery in active enhanced plaques.


  1. Darlington PJ, Touil T, Doucet JS, Gaucher D, Zeidan J, Gauchat D, et al. Diminished Th17 (not Th1) responses underlie multiple sclerosis disease abrogation after hematopoietic stem cell transplantation. Ann Neurol. 2013;73:341-54. doi: 10.1002/ana.23784. PubMed PMID: 23463494.
  2. T Jock Murray M. Multiple sclerosis: the history of a disease. Ne York: Demos medical publishing; 2004.
  3. Lutterotti A, Yousef S, Sputtek A, Sturner KH, Stellmann JP, Breiden P, et al. Antigen-specific tolerance by autologous myelin peptide-coupled cells: a phase 1 trial in multiple sclerosis. Sci Transl Med. 2013;5:188ra75. doi: 10.1126/scitranslmed.3006168. PubMed PMID: 23740901; PubMed Central PMCID: PMC3973034.
  4. Genain CP, Cannella B, Hauser SL, Raine CS. Identification of autoantibodies associated with myelin damage in multiple sclerosis. Nat Med. 1999;5:170-5. doi: 10.1038/5532. PubMed PMID: 9930864.
  5. Zajicek J, Fox P, Sanders H, Wright D, Vickery J, Nunn A, et al. Cannabinoids for treatment of spasticity and other symptoms related to multiple sclerosis (CAMS study): multicentre randomised placebo-controlled trial. Lancet. 2003;362:1517–26. doi: 10.1016/S0140-6736(03)14738-1.
  6. Bove R, Secor E, Healy BC, Musallam A, Vaughan T, Glanz BI, et al. Evaluation of an online platform for multiple sclerosis research: patient description, validation of severity scale, and exploration of BMI effects on disease course. PLoS One. 2013;8:e59707. doi: 10.1371/journal.pone.0059707. PubMed PMID: 23527256; PubMed Central PMCID: PMC3603866.
  7. Rossi S, Motta C, Studer V, Barbieri F, Buttari F, Bergami A, et al. Tumor necrosis factor is elevated in progressive multiple sclerosis and causes excitotoxic neurodegeneration. Mult Scler. 2014;20:304-12. doi: 10.1177/1352458513498128. PubMed PMID: 23886826.
  8. Krupp LB, Tardieu M, Amato MP, Banwell B, Chitnis T, Dale RC, et al. International Pediatric Multiple Sclerosis Study Group criteria for pediatric multiple sclerosis and immune-mediated central nervous system demyelinating disorders: revisions to the 2007 definitions. Mult Scler. 2013;19:1261-7. doi: 10.1177/1352458513484547. PubMed PMID: 23572237.
  9. Magliozzi R, Serafini B, Rosicarelli B, Chiappetta G, Veroni C, Reynolds R, et al. B-cell enrichment and Epstein-Barr virus infection in inflammatory cortical lesions in secondary progressive multiple sclerosis. J Neuropathol Exp Neurol. 2013;72:29-41. doi: 10.1097/NEN.0b013e31827bfc62. PubMed PMID: 23242282.
  10. Graham D, Huang S, Choi J, Rudin S, Yu D, Jenkins B, et al. ATX-MS-1467 reduces MRI lesions and prevents disease progression in a humanized mouse model of multiple sclerosis. MULTIPLE SCLEROSIS JOURNAL. 2014;20:235.
  11. Huang S, Choi J-K, Gray A, Yu D, Jenkins B, Mandeville J, et al. ONO-4641 (Ceralifimod) Reduces MRI Lesions and Prevents Disease Progression in an Animal Model of Multiple Sclerosis (P1. 219). Neurology. 2014;82:P1. 219.
  12. Giorgio A, Stromillo ML, Bartolozzi ML, Rossi F, Battaglini M, De Leucio A, et al. Relevance of hypointense brain MRI lesions for long-term worsening of clinical disability in relapsing multiple sclerosis. Mult Scler. 2014;20:214-9. doi: 10.1177/1352458513494490. PubMed PMID: 23877971.
  13. Coles AJ, Twyman CL, Arnold DL, Cohen JA, Confavreux C, Fox EJ, et al. Alemtuzumab for patients with relapsing multiple sclerosis after disease-modifying therapy: a randomised controlled phase 3 trial. Lancet. 2012;380:1829-39. doi: 10.1016/S0140-6736(12)61768-1. PubMed PMID: 23122650.
  14. Filippi M, Rocca MA, Ciccarelli O, De Stefano N, Evangelou N, Kappos L, et al. MRI criteria for the diagnosis of multiple sclerosis: MAGNIMS consensus guidelines. Lancet Neurol. 2016;15:292-303. doi: 10.1016/S1474-4422(15)00393-2. PubMed PMID: 26822746; PubMed Central PMCID: PMC4760851.
  15. Wens I, Dalgas U, Stenager E, Eijnde BO. Risk factors related to cardiovascular diseases and the metabolic syndrome in multiple sclerosis–a systematic review. Multiple Sclerosis Journal. 2013;19:1556-64. doi: 10.1177/1352458513504252 .
  16. Kolber P, Montag S, Fleischer V, Luessi F, Wilting J, Gawehn J, et al. Identification of cortical lesions using DIR and FLAIR in early stages of multiple sclerosis. J Neurol. 2015;262:1473-82. doi: 10.1007/s00415-015-7724-5. PubMed PMID: 25862481.
  17. Schmidt P, Gaser C, Arsic M, Buck D, Forschler A, Berthele A, et al. An automated tool for detection of FLAIR-hyperintense white-matter lesions in Multiple Sclerosis. Neuroimage. 2012;59:3774-83. doi: 10.1016/j.neuroimage.2011.11.032. PubMed PMID: 22119648.
  18. Patzig M, Burke M, Bruckmann H, Fesl G. Comparison of 3D cube FLAIR with 2D FLAIR for multiple sclerosis imaging at 3 Tesla. Rofo. 2014;186:484-8. doi: 10.1055/s-0033-1355896. PubMed PMID: 24347360.
  19. Absinta M, Vuolo L, Rao A, Nair G, Sati P, Cortese IC, et al. Gadolinium-based MRI characterization of leptomeningeal inflammation in multiple sclerosis. Neurology. 2015;85:18-28. doi: 10.1212/WNL.0000000000001587. PubMed PMID: 25888557; PubMed Central PMCID: PMC4501940.
  20. Tourdias T, Roggerone S, Filippi M, Kanagaki M, Rovaris M, Miller DH, et al. Assessment of Disease Activity in Multiple Sclerosis Phenotypes with Combined Gadolinium-and Superparamagnetic Iron Oxide–enhanced MR Imaging. Radiology. 2012;264:225-33. doi: 10.1148/radiol.12111416 .
  21. Lazeron RH, Langdon DW, Filippi M, van Waesberghe JH, Stevenson VL, Boringa JB, et al. Neuropsychological impairment in multiple sclerosis patients: the role of (juxta)cortical lesion on FLAIR. Mult Scler. 2000;6:280-5. doi: 10.1177/135245850000600410. PubMed PMID: 10962549.
  22. Castillo MS, Davis FG, Surawicz T, Bruner JM, Bigner S, Coons S, et al. Consistency of primary brain tumor diagnoses and codes in cancer surveillance systems. Neuroepidemiology. 2004;23:85-93. doi: 10.1159/000073980. PubMed PMID: 14739573.
  23. Gawne-Cain M, O’riordan J, Thompson A, Moseley I, Miller D. Multiple sclerosis lesion detection in the brain: a comparison of fast fluid-attenuated inversion recovery and conventional T2-weighted dual spin echo. Neurology. 1997;49:364-70. doi: 10.1212/wnl.49.2.364 .