Is Long-term Disability in Multiple Sclerosis Associated with Diffuse Cerebral Pathology Independent of Relapses?

Česká verzia

Authors: J. Piťha
Authors place of work: MS Centrum Teplice, Neurologické oddělení, Krajská zdravotní, a. s. – Nemocnice Teplice o. z.
Published in the journal: Cesk Slov Neurol N 2014; 77/110(1): 35-38
Category: Review Article

Summary

Development of disability in multiple sclerosis is traditional understood to be a consequence of accumulation of past relapses. New findings suggest that disability may also result from changes associated with diffuse cerebral pathology consequent to inflammatory and neurodegenerative changes in the normal-appearing white matter. The article attempts to answer questions related to immunopathological and morphological changes in the central nervous system leading to permanent disability.

Key words:
multiple sclerosis – relapse – disability – diffuse cerebral pathology

The author declares he has no potential conflicts of interest concerning drugs, products, or services used in the study.

The Editorial Board declares that the manuscript met the ICMJE “uniform requirements” for biomedical papers.

Zdroje

1. Compston A, Coles A. Multiple sclerosis. Lancet 2008; 372(9648): 1502–1517.

2. Kurschus FC, Wörtge S, Waisman A. Modeling a complex disease: multiple sclerosis. Adv Immunol 2011; 110: 111–137.

3. Lehmann-Horn K, Kronsbein HC, Weber MS. Targeting B cells in the treatment of multiple sclerosis: recent advances and remaining challenges. Ther Adv Neurol Disord 2013; 6(3): 161–173.

4. Horakova D, Kalincik T, Dusankova JB, Dolezal O. Clinical correlates of grey matter pathology in multiple sclerosis. BMC Neurol 2012; 12: 10.

5. Yoshida M, Hori M, Yokoyama K, Fukunaga I, Suzuki M, Kamagata K et al. Diffusional kurtosis imaging of normal-appearing white matter in multiple sclerosis: preliminary clinical experience. Jpn J Radiol 2013; 31(1): 50–55.

6. Caprariello AV, Mangla S, Miller RH, Selkirk SM. Apoptosis of oligodendrocytes in the central nervous system results in rapid focal demyelination. Ann Neurol 2012; 72(3): 395–405.

7. Lassmann H, van Horssen J, Mahad D. Progressive multiple sclerosis: pathology and pathogenesis. Nat Rev Neurol 2012; 8(11): 647–656.

8. Popescu V, Agosta F, Hulst HE, Sluimer IC, Knol DL, Sormani MP et al.; MAGNIMS Study Group. Brain atrophy and lesion load predict long term disability in multiple sclerosis. J Neurol Neurosurg Psychiatry 2013; 84(10): 1082–1091.

9. Lublin FD, Baier M, Cutter G. Effect of relapses on development of residual deficit in multiple sclerosis. Neurology 2003; 61(11): 1528–1532.

10. Weinshenker BG, Ebers GC. The natural history of multiple sclerosis. Can J Neurol Sci 1987; 14(3): 255–261.

11. Lublin FD, Reingold SC. Defining the clinical course of multiple sclerosis: results of an international survey. National Multiple Sclerosis Society (USA) Advisory Committee on Clinical Trials of New Agents in Multiple Sclerosis. Neurology 1996; 46(4): 907–911.

12. Wingerchuk DM, Hogancamp WF, O‘Brien PC, Weinshenker BG. The clinical course of neuromyelitis optica (Devic’s syndrome) Neurology 1999; 53(5): 1107–1114.

13. Bjartmar C, Kinkel RP, Kidd G, Rudick RA, Trapp BD. Axonal loss in normal-appearing white matter in a patient with acute multiple sclerosis. Neurology 2001; 57(7): 1248–1252.

14. DeLuca GC, Williams K, Evangelou N, Ebers GC, Esiri MM. The contribution of demyelination to axonal loss in multiple sclerosis. Brain 2006; 129(6): 1507–1516.

15. Trapp BD, Nave KA. Multiple sclerosis: an immune or neurodegenerative disorder? Annu Rev Neurosci 2008; 31: 247–269.

16. The IFNB Multiple Sclerosis Study Group. Interferon beta-1b is effective in relapsing-remitting multiple sclerosis. I. Clinical results of a multicenter, randomized, double-blind, placebo-controlled trial. Neurology 1993; 43)4): 655–661.

17. The IFNB Multiple Sclerosis Study Group and The University of British Columbia MS/MRI Analysis Group. Interferon beta-1b in the treatment of multiple sclerosis: final outcome of the randomized controlled trial. The IFNB Multiple Sclerosis Study Group and The University of British Columbia MS/MRI Analysis Group. Neurology 1995; 45(7): 1277–1285.

18. Jacobs LD, Cookfair DL, Rudick RA, Herndon RM, Richert JR, Salazar AM et al; The Multiple Sclerosis Collaborative Research Group (MSCRG). Intramuscular interferon beta-1a for disease progression in relapsing multiple sclerosis. Ann Neurol 1996; 39(3): 285–294.

19. European Study Group on interferon beta-1b in secondary progressive MS. Placebo-controlled multicentre randomised trial of interferon beta-1b in treatment of secondary progressive multiple sclerosis. Lancet 1998; 352(9139): 1491–1497.

20. PRISMS (Prevention of Relapses and Disability by Interferon beta-1a Subcutaneously in Multiple Sclerosis) Study Group. Randomised double-blind placebo- -controlled study of interferon beta-1a in relapsing/ remitting multiple sclerosis. Lancet 1998; 352(9139): 1498–1504.

21. Coles AJ, Wing MG, Molyneux P, Paolillo A, Davie CM, Hale G et al. Monoclonal antibody treatment exposes three mechanisms underlying the clinical course of multiple sclerosis. Ann Neurol 1999; 46(3): 296–304.

22. Comi G, Jeffery D, Kappos L, Montalban X, Boyko A, Rocca MA, Filippi M; ALLEGRO Study Group. Placeborelaps -controlled trial of oral laquinimod for multiple sclerosis. N Engl J Med 2012; 366(11): 1000–1009.

23. Confavreux C, Vukusic S, Moreau T, Adeleine P. Relapses and progression of disability in multiple sclerosis. N Engl J Med 2000; 343(20): 1430–1328.

24. Confavreux C, Vukusic S, Adeleine P. Early clinical predictors and progression of irreversible disability in multiple sclerosis: an amnesic process. Brain 2003; 126(4): 770–782.

25. Weinshenker BG, Bass B, Rice GP, Noseworthy J, Carriere W, Baskerville J et al. The natural history of multiple sclerosis: a geographically based study. I. Clinical course and disability. Brain 1989; 112(1): 133–146.

26. Kantarci O, Siva A, Eraksoy M, Karabudak R, Sutlas N, Agaoglu J et al; Turkish Multiple Sclerosis Study Group (TUMSSG). Survival and predictors of disability in Turkish multiple sclerosis patients. Neurology 1998; 51(3): 765–772.

27. Phadke JG. Clinical aspects of multiple sclerosis in north-east Scotland with particular reference to its course and prognosis. Brain 1990; 113(6): 1597–1628.

28. Kremenchutzky M, Cottrell D, Rice G, Hader W, Baskerville J, Koopman W et al. The natural history of multiple sclerosis: a geographically based study. Progressive-relapsing and relapsing-progressive multiple sclerosis: a re-evaluation. Brain 1999; 122(10): 1941–1950.

29. De Stefano N, Narayanan S, Francis SJ, Smith S, Mortilla M, Tartaglia MC et al. Diffuse axonal and tissue injury in patients with multiple sclerosis with low cerebral lesion load and no disability. Arch Neurol 2002; 59(10): 1565–1571.

30. Popescu BF, Bunyan RF, Parisi JE, Ransohoff RM, Lucchinetti CF. A case of multiple sclerosis presenting with inflammatory cortical demyelination. Neurology 2011; 76(20): 1705–1710.

31. Filippi M, Rocca MA, Barkhof F, Brück W, Chen JT, Comi G et al; Attendees of the Correlation between Pathological MRI findings in MS workshop.. Association between pathological and MRI findings in multiple sclerosis. Lancet Neurol 2012; 11(4): 349–360.

32. Markiewicz I, Lukomska B. The role of astrocytes in the physiology and pathology of the central nervous system. Acta Neurobiol Exp 2006; 66(4): 343–358.

33. Sofroniew MV. Molecular dissection of reactive astrogliosis and glial scar formation. Trends Neurosci 2009; 32(12): 638–647.

34. Cambron M, D’Haeseleer M, Laureys G, Clinckers R, Debruyne J, De Keyser J. White-matter astrocytes, axonal energy metabolism, and axonal degeneration in multiple sclerosis. J Cereb Blood Flow Metab 2012; 32(3): 413–424.

35. Bjartmar C, Kinkel RP, Kidd G, Rudick RA, Trapp BD. Axonal loss in normal-appearing white matter in a patient with acute MS. Neurology 2001; 57(7): 1248–1252.

36. Evangelou N, Esiri MM, Smith S, Palace J, Matthews PM. Quantitative pathological evidence for axonal loss in normal appearing white matter in multiple sclerosis. Ann Neurol 2000; 47(3): 391–395.

37. Kirov II, Patil V, Babb JS, Rusinek H, Herbert J, Gonen O. Spectroscopy indicates diffuse multiple sclerosis activity during remission. J Neurol Neurosurg Psychiatry 2009; 80(12): 1330–1336.

38. Fialová L, Bartos A, Švarcová J, Zimova D, Kotoucova J. Serum and cerebrospinal fluid heavy neurofilaments and antibodies against them in early multiple sclerosis. J Neuroimmunol 2013; 15: 259(1–2): 81–87.

39. Lublin FD. Relapses do not matter in relation to long-term disability: no (they do). Mult Scler 2011; 17(12): 1415–1416.

40. Popescu V, Agosta F, Hulst HE, Sluimer IC, Knol DL, Sormani MP et al; MAGNIMS Study Group. Brain atrophy and lesion load predict long term disability in multiple sclerosis. J Neurol Neurosurg Psychiatry 2013; 84(10): 1082–1091.

41. Fisniku LK, Brex PA, Altmann DR, Miszkiel KA, Benton CE, Lanyon R et al. Disability and T2 MRI lesions: a 20-year follow-up of patients with relapse onset of multiple sclerosis. Brain 2008; 131(3): 808–817.

42. Confavreux C, Vukusic S, Moreau T, Adeleine P. Relapses and progression of disability in multiple sclerosis. N Engl J Med 2000 16; 343(20):1430–1438.

43. Casserly C, Ebers GC. Relapses do not matter in relation to long-term disability: yes. Mult Scler 2011; 17(12): 1412–1424.

44. Tremlett H, Yousefi M, Devonshire V, Rieckmann P, Zhao Y; UBC Neurologists. Impact of multiple sclerosis relapses on progression diminishes with time. Neurology 2009; 73(20): 1616–1623.

45. Scalfari A, Neuhaus A, Daumer M, Deluca GC, Muraro PA, Ebers GC. Early relapses, onset of progression, and late outcome in multiple sclerosis. JAMA Neurol 2013; 70(2): 214–222.

46. Rocca MA, Messina R, Filippi M. Multiple sclerosis imaging: recent advances. J Neurol 2013; 260(3): 929–935.

47. Meier DS, Weiner HL, Guttmann CR. Time-series modeling of multiple sclerosis disease activity: a promising window on disease progression and repair potential? Neurotherapeutics 2007; 4(3): 485–498.