Primary Progressive Multiple Sclerosis by M. Filippi, M. Rovaris, G. Comi (auth.), Massimo Filippi,

By M. Filippi, M. Rovaris, G. Comi (auth.), Massimo Filippi, Giancarlo Comi (eds.)

"Why are there no powerful remedies for my ? Why do researchers exclude sufferers with fundamental revolutionary a number of sclerosis from enrolling in medical trials? Please allow me recognize should you pay attention of reviews that i'd be allowed to go into or remedies that i'll attempt for my . " therefore, lately, the unhappy lament of the sufferer with basic innovative MS (PPMS). This variation, frequently within the guise of a protracted innovative myelopathy or, much less quite often, innovative cerebellar or bulbar disorder, often responds poorly to corticosteroids and barely turns out to profit to an important measure from extensive immunosuppressive remedies. lately, so much randomized clin­ ical trials have excluded PPMS sufferers on counts. scientific worsening devel­ ops slowly in PPMS and should no longer be famous through the process a 2-or 3-year trial even in untreated keep watch over sufferers. This issue on my own provides to the possibility of a kind 2 blunders or, a minimum of, inflates the pattern dimension and period of the trial. moreover, there's mounting facts that revolutionary axonal degeneration and neuronal loss (rather than lively, recurrent irritation) will be very important elements of the pathology during this kind of the ailment. even though modern trials are comparing even if PPMS sufferers could benefit from remedy with the ~-interferons and glatiramer acetate, initial, out of control medical experi­ ence means that the implications is probably not dramatic.

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Trinchieri G (1995) Interleukin 12: a proinflammatory cytokine with immunoregulatory functions that bridge innate resistance and antigen-specific adaptive immunity. Annu Rev Immunol13:251-276 23. Correale J, McMillan M, Li S et al (1997) Antigen presentation by autoreactive proteolipid protein peptide-specific T cell clones from chronic progressive multiple sclerosis patients: roles of co-stimulatory B7 molecules and IL-12. J Neuroimmunol72:27-43 24. Comabella M, Balashov K, Issazadeh S et al (1998) Elevated interleukin-12 in progressive multiple sclerosis correlates with disease activity and is normalized by pulse cyclophosphamide therapy.

The role offrontallobe pathology. Brain 120:15-26 52. Rovaris M, Filippi M, Falautano M et al (1998) Relationship between MR abnormalities and patterns of cognitive impairment in multiple sclerosis. Neurology 50:1601-1608 53. Heaton RK, Nelson LM, Thompson DS et al (1985) Neuropsychological findings in relapsing-remitting and chronic-progressive multiple sclerosis. J Consult Clin Psychol 53:103-110 54. Beatty WW, Goodkin DE, Monson N, Beatty PA (1989) Cognitive disturbances in patients with relapsing remitting multiple sclerosis.

McGavern DB, Murray PD, Rivera-Quinones C et al (2000) Axonal loss results in spinal cord atrophy, electrophysiological abnormalities and neurological deficits following demyelination in a chronic inflammatory model of multiple sclerosis. Brain 123:519-531 17. Gronseth GS, Ashman EJ (2000) Practice parameter: the usefulness of evoked potentials in identifying clinically silent lesions in patients with suspected multiple sclerosis (an evidence-based review): report of the Quality Standards Subcommittee'of the American Academy of Neurology.

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