New treatments have radically changed the course and survival rate of MS, resulting in progressively fewer relapses and hospitalisations and slower disease progression. However, despite major advances, all available treatments are only partially effective - there is currently no cure for MS. Treatments either target individual symptoms or aim to modify disease progression. Symptomatic treatments do not alter the course of the disease and vary both inter- and intra-individually depending on the presenting complaint(s) at a given point in time. These might include muscle relaxants such as baclofen to relieve painful or uncomfortable muscle stiffness or spasms, antidepressant medications such as fluoxetine to treat affective disorders, and physical therapies to assist in the performance of everyday activities. These are critical in the care of MS patients, enhancing quality of life, and capacity to work. Treatments for MS attacks, or relapses, focus on shortening the length of the relapse and hastening recover)'. Oral (prednisone) and intravenous (methylpred- nisolone) corticosteroids are most commonly used, altering the immune response by reducing inflammation. In more severe cases plasmapheresis may be used, the replacement of the blood’s plasma thought to remove the circulating antibodies active in MS.

Disease-modifying treatments, as the name suggests, aim to halt or slow down progression of the underlying disease. Over recent years these have progressed from broad spectrum immunosuppressants, to immunomodulators, to ill-defined immunostimulants, to more selective, continuous immunosuppressants. As of January 2018, the Therapeutic Goods Administration had approved 12 of these medications for use in RRMS in Australia. These are four preparations of interferon beta, which has been at the forefront of disease management in MS for more than 20 years, glatiramer acetate, the monoclonal antibodies natalizumab, alemtuzumab, and daclizumab, the first B-cell-targeted therapy, ocrelizumab, and the small-molecule oral agents fingolimod, dimethyl fumarate, and teriflunomide. All reduce, to varying degrees, the likelihood of the development of new lesions, relapses, and stepwise accumulation of disability. First-line treatments are usually interferon-beta, glatiramer acetate or teriflunomide. Escalation treatments (natalizumab, fingolimod and mitoxantrone) are more potent than first-line treatments, although have potentially serious side effects.

Currently, there are no specific pharmacological treatments for cognitive impairment in MS, and only limited and inconsistent evidence to suggest that disease modifying therapies have any influence on the development and progression of deficit (Niccolai, Goretti & Amato, 2017). An emerging field gathering considerable interest is cognitive rehabilitation, which aims to improve cognitive functioning through specifically designed training programs, or through teaching compensatory strategies to offset the impact of cognitive deficits on day-to-day life. However, the efficacy of cognitive rehabilitation approaches is currently questionable (Mitolo, Venneri, Wilkinson & Sharrack, 2015; Rosti-Otajarvi & Hamalainen, 2014), in part due to the lack of theoretical and physiological models of cognitive impairment in MS.

Concluding remarks

The last two decades have witnessed unprecedented activity and interest in MS. Yet MS remains among the most challenging of all neurologic disorders, with a largely unknown aetiology, and a highly heterogeneous and variable clinical course. While all approved drugs predominantly exert their effects on the inflammatory component of the disease, no drug so far significantly improves the degenerative disease process. The real breakthrough in the treatment of MS will therefore come with the identification and application of treatments that can also prevent neurodegeneration as well as support remyelination and repair of damaged tissue.


APN acquired pendular nystagmus

BVMT-R Brief Visuospatial Memory Test-Revised

CDMS clinically definite multiple sclerosis

CIS clinically isolated syndrome

CNS central nervous system

CSF cerebrospinal fluid

CVLT-II California Verbal Learning Test-II

EBV Epstein-Barr virus

EDSS Expanded Disability Severity Scale

HLA human leukocyte antigens

IgG immunoglobulin

IL-2RA interleukin 2 receptor A

IL7R interleukin 7 receptor

INO internuclear ophthalmoparesis

MRI magnetic resonance imaging

MS multiple sclerosis

MSFC multiple sclerosis functional composite

OCT optical coherence tomography

ON optic neuritis

PAS AT Paced Auditory Serial Addition Test PPMS primary progressive multiple sclerosis

SDMT Symbol Digit Modalities Test

SPMS secondary progressive multiple sclerosis VEP visual evoked potentials

Further reading

Benedict, R. H. B., DeLuca, J., Phillips, G., LaRocca, N., Hudson, L. D., Rudick, R. & Multiple Sclerosis Outcome Assessments Consortium. (2017). Validity of the Symbol Digit Modalities Test as a cognition performance outcome measure for multiple sclerosis. Multiple Sclerosis Journal, 23(5), 721-733.

Brownlee, W. J., Hardy, T. A., Fazekas, F. & Miller, D. H. (2017). Diagnosis of multiple sclerosis: progress and challenges. Lancet, 3X9(10076), 1336-1346.

Fielding, J., Clough, M., Millist, L., Beh, S., Sears D., Frohman, A., Renneker, R., Lim, J., Lizak, N., Frohman, T., White, O. & Frohman, E. (2015). Ocular motor pathophysiological signatures of cognitive dysfunction in multiple sclerosis. Nature Reviews Neurology, i 1, 637-645.

Matthews, P. M., Roncaroli, F., Waldman, A., Sormani, M. P., De Stefano, N., Giovannoni, G. & Reynolds, R. (2016). A practical review of the neuropathology and neuroimaging of multiple sclerosis. Practical Neurology, 16(4), 279-287.

Rocca, M. A., Amato, M. P., De Stefano, N., Enzinger, C., Geurts, J. J., Penner, I. K.,

. . . MAGNIMS Study Group. (2015). Clinical and imaging assessment of cognitive dysfunction in multiple sclerosis. Lancet Neurology, 14(3), 302-317.

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