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Multiple Sclerosis in its European Matrix: Some Aspects of History, Mechanisms and Treatment

Published online by Cambridge University Press:  02 December 2014

Ian McDonald
Ian McDonald*
Affiliation:
Royal College of Physicians of London, London, UK
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Abstract

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Susceptibility to multiple sclerosis is influenced by several genes which are relatively common in populations of European origin. Their precise identification is currently being intensively investigated. The pathophysiology of the main clinical features is better understood. Relapse results from abnormalities of conduction to which both demyelination and inflammation contribute. At the membrane level, remission depends on the formation of new sodium channels which restore conduction even in persistently demyelinated axons. Remyelination presumably contributes and synaptic reorganisation may also do so. Axonal degeneration contributes to irrecoverable deficit and progression of disability. These observations suggest new therapeutic strategies. The management of multiple sclerosis needs to be improved. Progress requires an ethically based partnership between patients, whose needs are paramount, the research and caring communities and the pharmaceutical industry.

Type
Review Article
Information
Canadian Journal of Neurological Sciences , Volume 31 , Issue 1 , February 2004 , pp. 37 - 47
Copyright
Copyright © The Canadian Journal of Neurological 2004

References

1.Poser, CM.The dissemination of multiple sclerosis: a Viking saga? A historical essay. Ann Neurol 1994; 36 (Suppl 2): S231-S243.Google Scholar
2.Fredrickson, S, Kam-Hausen, S.The 150-year anniversary ofmultiple sclerosis: does its early history give an aetiological clue? Perspect Biol Med 1989; 32: 237–243.CrossRefGoogle Scholar
3.Compston, A.Genetic susceptibility to multiple sclerosis. In: Compston, A, Ebers, G, Lassmann, H, et al. McAlpine’s Multiple Sclerosis. 3rd ed. London: Churchill Livingstone, 1998: 101–142.Google Scholar
4.Firth, D.The Case of Augustus d’Este. Cambridge: Cambridge University Press, 1948.Google Scholar
5.Gillen, M.Royal, Duke.Augustus Frederick, Duke of Sussex (1773–1843). London: Sedgwick & Jackson, 1976.Google Scholar
6.Gibbon, E.Antiquities of the House of Brunswick. In: Miscellaneous Works of Edward Gibbon Esquire, with memoirs of his life and writings composed by himself: illustrated from his letters with occasional notes and narrative by John Lord Sheffield. Vol II. London: printed for A Strathan and T Cadell Jr. and W Davies(Successor to Mr Cadell), 1796: 701–702.Google Scholar
7.Paget, G.The lineage and ancestry of H.R.H. Prince Charles, Prince of Wales. Edinburgh: Skilton: 2 vols, 1977.Google Scholar
8.Carswell, R.Pathological Anatomy: Illustrations of the Elementary Forms of Disease. London: Orme, Brown, Green & Longman: 1838.Google Scholar
9.Charcot, J-M.Histologie de la sclérose en plaques. Gaz. Hôpital(Paris) 1868; 41: 554–566.Google Scholar
10.Sadovnick, AD, Armstrong, H, Rice, GPA, et al. A population-basedstudy of multiple sclerosis in twins: update. Ann Neurol 1993; 33:281–285. Google Scholar
11.Munford, CJ, Wood, NW, Keller-Wood, HF, et al. The British Islessurvey of multiple sclerosis in twins. Neurology 1994; 44: 11–15.CrossRefGoogle Scholar
12.French, Research Group on Multiple sclerosis. Multiple sclerosis in 54 twinships: concordance rate is independent of zygosity. Ann Neurol 1992; 32: 724–727.Google Scholar
13.Compston, A.Distribution of multiple sclerosis. In: Compston, A, Ebers, G, Lassmann, H, et al. McAlpine’s Multiple Sclerosis. 3rd ed. London: Churchill Livingstone, 1998: 63–100.Google Scholar
14.Hammond, SR, English, DR, McLeod, JG.The age-range of risk ofdeveloping multiple sclerosis: evidence froma migrantpopulation in Australia. Brain 2000; 123: 968–974.Google Scholar
15.Granieri, E, Casseta, I, Govoni, V, et al. The increasing incidence andprevalence of MS in a Sardinian province. Neurology 2000; 55: 842–847.CrossRefGoogle Scholar
16.Sawcer, S, Jones, HB, Feakes, R, et al. A genome screen in multiplesclerosis reveals susceptibility loci on chromosome 6p21 and17q22. Nature Genet 1996; 13: 464–468.CrossRefGoogle Scholar
17.Ebers, GC, Kukey, K, Bulman, AE, et al. A full genome search inmultiple sclerosis. Nature Genet 1996; 13(4): 472–476.Google Scholar
18.Multiple Sclerosis Genetics Group. A complete genomic screen formultiple sclerosis underscores a role for the major histocompatibility complex. Nature Genet 1996; 51: 748–753.Google Scholar
19.Hugot, J-P, Chamaillard, M, Zoualis, H, et al. Association of NOD2leucine-rich repeat variants with susceptibility to Crohn’s disease. Nature 2001; 411: 599–603.Google Scholar
20.Ogura, Y, Boneri, DK, Inohann, N, et al. A frame shift mutation ofNOD2 associated with susceptibility to Crohn’s disease. Nature 2001; 411: 603–606.CrossRefGoogle ScholarPubMed
21.McDonald, WI.The effects of experimental demyelination onconduction in peripheral nerve: A histological and electrophysiological study. II. Electrophysiological observations. Brain 1963; 86: 501–534.CrossRefGoogle ScholarPubMed
22.McDonald, WI, Sears, TA.The effects of experimental demyelinationon conduction and the central nervous system. Brain 1970; 93:583–598.Google Scholar
23.Halliday, AM, McDonald, WI, Mushin, J.Delayed visual evokedresponse in optic neuritis. Trends Neurosci 1972; 20: 63–67.Google Scholar
24.Halliday, AM, McDonald, WI, Mushin, J.Visual evoked response indiagnosis of multiple sclerosis. Br Med 1973; 4: 661–664.Google Scholar
25.Berry, K, Paty, DW.Correlation between NMR scan and brain slicedata in multiple sclerosis. Lancet 1984;ii:412.Google Scholar
26.Kermode, AG, Thompson, AJ, Tofts, P, et al. Breakdown of the blood-brain barrier precedes symptoms and other MRI signs of new lesions in multiple sclerosis. Pathogenetic and clinical implications. Brain 1990; 113: 1477–1489.Google Scholar
27.Thompson, AJ, Kermode, AG, Wicks, D, et al. Major differences inthe dynamics of primary and secondary progressive multiplesclerosis. Ann Neurol 1991; 29: 53–62.CrossRefGoogle Scholar
28.Katz, D, Taubenberger, JK, Cannella, B, et al. Correlation between magnetic resonance imaging findings and lesion development in chronic, active multiple sclerosis. Ann Neurol 1993; 34: 661–669.Google Scholar
29.Johnson, G, Miller, DH, MacManus, D, et al. STIR sequences inNMR imaging of the optic nerve. Neuroradiology 1987; 29: 238–245.CrossRefGoogle ScholarPubMed
30.Youl, BD, Turano, G, Miller, H, et al. The pathophysiology of acuteoptic neuritis. An association of gadolinium leakage with clinical and electrophysiological deficits. Brain 1991; 114: 2437–2450.Google Scholar
31.Smith, KJ, McDonald, WI.The pathophysiology of multiplesclerosis: the mechanisms underlying the production of symptoms and the natural history of the disease. Phil Trans R SocLond 1999; 354: 1649–1673.Google Scholar
32.Smith, KJ, Kapoor, R, Hall, SM, Davies, M.Electrically active axonsdegenerate when exposed to nitric oxide. Ann Neurol 2001; 49:470–476.CrossRefGoogle ScholarPubMed
33.Moll, C, Mourre, C, Lazdunski, M, et al. Increase of sodium channelsin demyelinated lesions of multiple sclerosis. Brain Res 1991;556: 311–316.CrossRefGoogle Scholar
34.Werring, DJ, Bullmore, ET, Toosy, AT, et al. Recovery from opticneuritis is associated with a change in the distribution of cerebral response to visual stimulation: a functional magnetic resonance imaging study. J Neurol Neurosurg Psychiatry 2000; 68: 441–449.Google Scholar
35.Lee, M, Reddy, H, Johansen-Berg, H, et al. The motor cortex showsadaptive functional changes to brain injury from multiplesclerosis. Ann Neurol 2000; 47: 606–613.Google Scholar
36.Cifelli , A, Matthews, PM.Cerebral plasticity in multiple sclerosis. Multiple Sclerosis 2002; 8:193–199.CrossRefGoogle ScholarPubMed
37.Lassmann, H, Suchanekg, Ozawa K.Histopathology and blood-cerebrospinal fluid barrier in multiple sclerosis. Ann Neurol 1994; 36: S42-S46.Google Scholar
38.Kornek, B, Lassmann, H.Axonal pathology in multiple sclerosis. Ahistorical note. Brain 1999; 9: 651–656.Google Scholar
39.Ferguson, B, Matyszak, M, Esiri, MM, Perry, VH.Axonal damage inacute multiple sclerosis lesions. Brain 1997; 120: 393–399.Google Scholar
40.Trapp, BD, Peterson, J, Ransohoff, RM, et al. Axonal transaction inthe lesions of multiple sclerosis. N Engl J Med 1998; 378: 278–285.Google Scholar
41.Losseff, MA, Webb, SL, O’Riordan, JI, et al. Spinal cord atrophy anddisability in multiple sclerosis. A new reproducible and sensitive MRI method with potential to monitor disease progression. Brain 1996; 119: 701–708.CrossRefGoogle Scholar
42.Davie, CA, Barker, GJ, Webb, S, et al. Persistent functional deficit inmultiple sclerosis and autosomal dominant cerebellar ataxia is associated with axon loss. Brain 1995; 118: 1583–1592.Google Scholar
43.Bolanos, JP, Almeida, A, Stewart, V, et al. Nitric oxide-mediatedmitochondrial damage in the brain: mechanisms and implications for neurodegenerative diseases. J Neurochem 1997; 68: 2227–2240.Google Scholar
44.Bostock, H, Grafe, P.Activity-dependent excitability changes innormal and demyelinated rat spinal axons. J Physiol 1985; 365:Google Scholar
45.Li, S, Jiang, U, Stys, PK.Important role of reverse Na+-Ca++ exchangein spinal cord white matter injury at physiological temperature. J Neurophysiol 2000; 84: 1116–1119.Google Scholar
46.Smith, KJ, Blaker, PA, Kapoor, R, et al. Protection of axons fromdegeneration resulting from exposure to nitric oxide. J Neurol Neurosurg Psychiatry 2001; 70: 282.Google Scholar
47.Smith, KJ, Kapoor, R, Hall, SM, Davies, M.Partial sodium channelblockage protects axons from degeneration caused by the combination of impulse activity and exposure to nitric oxide. Society for Neuroscience Abstracts 2001; 103:12.Google Scholar
48.Johnson, S.Quoted by Wiltshire J in: Samuel Johnson in the Medical World. Cambridge: Cambridge University Press, 1991.Google Scholar
49.Matthews, JR.Quantification and the quest for medical certainty. Princeton, New Jersey: Princeton University Press, 1995.Google Scholar
50.Louis, P-C-A. Pathological researches on phthisis. Trans. Charles Cowan. Boston: Hilliard Grey, 1836. Cited by Matthews in ref. 49.Google Scholar
51.Radicke, G.On the importance and value of arithmetic means; withspecial reference to recent physiological researches on the determination of the influence of certain agencies upon the metamorphosis of tissue; with rules for accurately estimating the same. Trans. FT Bond. London: The New Sydenham Society, 1861.Google Scholar
52.Greenwood, M.On methods of research available in the study of medical problems. With special reference to Sir Almroth Wright’s recent utterances. Lancet 1913; I: 158–165.Google Scholar
53.Dunnill, M.The Plato of Praed Street. The Life and Times ofAlmroth Wright. London: Royal Society of Medicine Press, 2000.Google Scholar
54.Fisher, RA.The Design of Experiments. Edinburgh: Oliver & Boyd, 1935.Google Scholar
55.MRC. Streptomycin treatment of pulmonary tuberculosis. A MRCinvestigation. Brit Med J 1948; II: 769–782.Google Scholar
56.Marshall, EK.Clinical therapeutic trial of a new drug. Bull JohnsHopkins Hosp 1949; 85:221–230.Google Scholar
57.Rose, AS, Kuzma, JW, Kurtzke, JF, et al. Co-operative study in theevaluation of therapy in multiple sclerosis: ACTH vs. placebo: final report. Neurology 1970; 20 (part 2): 1–19.Google Scholar
58.Weiner, HL, Ellison, GW.A working protocol to be used as aguideline for trials in multiple sclerosis. Arch Neurol 1983; 40:704–710.Google Scholar
59.IFNB Multiple Sclerosis Study Group. Interferon beta-1b iseffective in relapsing, hyper-remitting multiple sclerosis. I. Clinical results of a multi-centre, randomised, double-blind, placebo-controlled trial. Neurology 1993; 43: 655–661.Google Scholar
60.Paty, DW, Li, DKB, IFNB Multiple Sclerosis Study Group. Interferon beta-1b is effective in relapsing, hyper-remitting multiple sclerosis. II. MRI results of a multi-centre, randomised, double-blind, placebo-controlled trial. Neurology 1993; 43: 662–667.Google Scholar
61.Johnson, KP, Brooks, BR, Cohen, JA, et al. Copolymer I reducesrelapse rate and improves disability in relapsing-remitting multiple sclerosis: results of a phase III multi-centre, double-blind, placebo-controlled trial. Neurology 1995; 45: 1268–1276.Google Scholar