Secondary progressive multiple sclerosis

SPMS is defined as the progressive accumulation of disability after an initial relapsing course, with or without occasional relapses and minor remissions¹

Active disease may be defined clinically or on imaging¹:

• Clinical: relapses, acute or subacute episodes of new or increasing neurologic dysfunction followed by full or partial recovery, in the absence of fever or infection.
• Imaging (MRI): occurrence of contrast-enhancing T1 hyperintense or new or unequivocally enlarging T2 hyperintense lesions.

SPMS may be a result of inflammation that accumulates from the start^2–5

Peripherally driven inflammation²

• Occurs when circulating immune cells temporarily damage the brain²
• Leads to relapses²

Central inflammation and neurodegeneration^2,3

• The activation of CNS-resident immune cells is independent of peripheral inflammation and can worsen when immune cells become trapped after crossing the blood-brain barrier^2,3
• May lead to neurodegeneration, irreversibly damaging white and grey matter²

In most clinical contexts, signs of transition are often unclear and SPMS is diagnosed retrospectively^6,7

When transitioning to SPMS, patients may notice a range of changes in disability.

Patients with lower relapse frequency but increasing disability could be transitioning to SPMS.

SPMS, secondary progressive multiple sclerosis.

Many patients will progress along the MS spectrum to SPMS¹⁰

^†From an analysis of 14,211 patients with MS. Amongst the 3169 patients who had at least 10 years of observation, 723 reached SPMS.¹¹

DMTs, disease-modifying therapies; RRMS, relapsing-remitting multiple sclerosis; SPMS, secondary progressive multiple sclerosis.

CNS, central nervous system; MRI, magnetic resonance imaging; MS, multiple sclerosis; RRMS, relapsing-remitting multiple sclerosis; SPMS, secondary progressive multiple sclerosis.

References

1. Lublin FD et al. Neurology. 2014;83:278–286.
2. Dendrou CA et al. Nat Rev Immunol. 2015;15:545–558.
3. Kutzelnigg A et al. Brain. 2005;128(Pt 11):2705–2712.
4. Ziemssen T et al. J Neurol. 2016;263:1053–1065.
5. Lassman H et al. Nat Rev Neurol. 2012;8(11):647–656.
6. Sumowski JF et al. Neurology. 2018;90:278–288.
7. Amato MP et al. J Neurol. 2013;260:1452–1468.
8. Gross HJ, Watson C. Neuropsychiatr Dis Treat. 2017;13:1349–1357.
9. Achiron A et al. J Neurol Neurosurg Psychiatry. 2005;76:744–749.
10. Larochelle C et al. Trends Neurosci. 2016;39(5):325–339.
11. Khurana V, Medin J. Poster presented at: the 7th Joint ECTRIM-ACTRIMS Meeting, 25–28 October 2017, Paris, France.
12. Bergamaschi R et al. Eur J Neurol. 2015. 22(6):981–989.