Multiple sclerosis

Published on 03/03/2015 by admin

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Last modified 22/04/2025

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Chapter 2

Multiple sclerosis

Definitions

Multiple sclerosis (MS) is defined as a chronic, inflammatory, demyelinating auto-immunological disease. The name multiple sclerosis refers to the scars (sclerosis), known as plaques, formed in the nervous system. There are four types of MS classified according to the course/progression of the disease process.

Aetiology

The definitive cause is unknown. However, the evidence suggests that the cause may be a combination of both genetic and environmental factors.

Pathology

Although the initial trigger is unknown, the damage to the nervous system in MS is believed to be caused by the patient’s own immune system. Lesions most commonly involve the white matter of the central nervous system in a process of demyelination. The peripheral nervous system is rarely involved.

The process of demyelination

The process of demyelination appears complex with the end result being damage or destruction of the oligodendrocytes in the central nervous system by lymphocytes (white blood cells) in the immune system. This results in an inflammatory response which stimulates other immune cells, causing a number of other damaging effects such as swelling, activation of macrophages and other destructive proteins and a change in the blood–brain barrier integrity. Unlike the peripheral nervous system, damage to central nervous system is not followed by extensive regeneration as it is limited by hostile glial cells and the extracellular environment. Nevertheless, some remyelination has been found to take place in the early phases of the disease. Repeated attacks however, lead to successively fewer effective remyelinations, until a scar-like plaque (sclerosis) is built up around the damaged axons.

Outcome and prognosis

The process of demyelination results in a thinning or complete loss of myelin (Fig. 2.1) and as the disease advances, the destruction of the nerve axons. The nervous system depends crucially on the myelin sheath for insulation and support and for fast nerve conduction (S2.6) so that when the myelin is lost, the neuron no longer conducts electrical signals effectively. Of course with axon destruction, it is impossible for the neuron to conduct signals. The outcome of these processes means that communication between different parts of the central nervous system is slow, inaccurate or non-functional.

The life expectancy of an individual with MS is more or less normal. However, the mortality for older patients and those with longer disease duration is slightly higher in MS patients.

Signs and symptoms

MS is an extremely variable condition. Signs and symptoms develop as the cumulative result of multiple lesions in the central nervous system. Sites of demyelination include the cerebral cortex, brain stem, spinal cord, basal ganglia, cerebellum and the cranial nerves. Understanding the function of these different areas of the brain (S2.7, 9, 10, 11, 12, 13, 14, 15) will give the therapist a platform by which to reason the potential clinical presentation.

The signs and symptoms presented will be a complex array of:

References and Further Reading

Alonso, A, Jick, SS, Olek, MJ, et al. Incidence of multiple sclerosis in the United Kingdom: findings from a population-based cohort. Journal of Neurology. 2007; 254:1736–1741.

Ascherio, A, Munger, KL. Environmental risk factors for multiple sclerosis. Part I: the role of infection. Annals of Neurology. 2007; 61:288–299.

Ascherio, A, Munger, KL. Environmental risk factors for multiple sclerosis. Part II: noninfectious factors. Annals of Neurology. 2007; 61:504–513.

Aulchenko, YS, Hoppenbrouwers, IA, Ramagopalan, SV, et al. Genetic variation in the KIF1B locus influences susceptibility to multiple sclerosis. Nature Genetics. 2008; 40:1402–1403.

Chari, DM. Remyelination in multiple sclerosis. International Review of Neurobiology. 2007; 79:589–620.

Christensen, T. Human herpes viruses in MS. International MS Journal. 2007; 14:41–47.

Compston, A, Coles, A. Multiple sclerosis. Lancet. 2002; 359:1221–1231.

Filippi, M, Bozzali, M, Rovaris, M, et al. Evidence for widespread axonal damage at the earliest clinical stage of multiple sclerosis. Brain. 2003; 126:433–437.

Islam, T, Gauderman, J, Cozen, W, et al. Differential twin concordance for multiple sclerosis by latitude of birthplace. Annals of Neurology. 2006; 60:56–64.

Lünemann, JD, Kamradt, T, Martin, R, et al. Epstein Barr virus: environmental trigger of multiple sclerosis. Journal of Virology. 2007; 81:6777–6784.

Marrie, RA. Environmental risk factors in multiple sclerosis aetiology. Lancet: Neurology. 2004; 3:709–718.

MS Society www.mssociety.org

Munger, KL, Levin, LI, Hollis, BW, et al. Serum 25-hydroxyvitamin D levels and risk of multiple sclerosis. Journal of the American Medical Association. 2006; 296:2832–2838.

Pascual, AM, Martínez-Bisbal, MC, Boscá, I, et al. Axonal loss is progressive and partly dissociated from lesion load in early multiple sclerosis. Neurology. 2007; 69:63–67.

Ragonese, P, Aridon, P, Salemi, G. Mortality in multiple sclerosis: a review. European Journal of Neurology. 2008; 15:123–127.

Ramsaransing, GS, De Keyser, J. Benign course in multiple sclerosis: a review. Acta Orthopaedica Scandinavica. 2006; 113:359–369.

Royal College of Physicians. Multiple sclerosis: national clinical guideline for diagnosis and management in primary and secondary care. www.rcplondon.ac.uk, 2004.

Svejgaard, A. The immunogenetics of multiple sclerosis. Immunogenetics. 2008; 60:275–286.

Waubant, E. Biomarkers indicative of blood-brain barrier disruption in multiple sclerosis. Disease Markers. 2006; 22:235–244.

Weber, F, Fontaine, B, Cournu-Rebeix, I, et al. IL2RA and IL7RA genes confer susceptibility for multiple sclerosis in two independent European populations. Genes and Immunity. 2008; 9:259–263.

World Health Organization. Neurological disorders: a public health challenge. www.who.int/mental_health/neurology/neurological_disorders_report_web.pdf, 2006.